Zobair Younossi, MD, MPH, is chairman of the Global NASH/MASH Council and professor and chairman of Beatty Liver and Obesity Research at Inova Health System.

From Validation to Implementation: Scaling NITs in MASLD Care, With Zobair Younossi, MD, MPH

As the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to climb in parallel with obesity and type 2 diabetes, clinicians face a pressing question regarding how at-risk patients should be identified and managed in routine practice.

Although noninvasive tests (NITs) have been validated for fibrosis risk stratification and are increasingly incorporated into society guidelines, their adoption remains inconsistent across care settings. At the same time, therapeutic options for metabolic dysfunction-associated steatohepatitis (MASH) are expanding, raising the stakes for early and accurate case finding. Against this backdrop, the conversation is shifting from whether to use noninvasive testing to how quickly and broadly it should be implemented and what barriers must be addressed to make risk-based MASLD care a standard part of clinical workflows.

, Zobair Younossi, MD, MPH, professor and chairman of the Global NASH Council, makes a clear and urgent case that the time to implement NIT-based risk stratification for MASLD is now.

Check out part 1 of the interview with Younossi 

While no test is perfect, he argues the data are sufficiently strong to support widespread adoption across clinical settings, most recently from his trio of sequentially published papers on how NITs perform across regions, how well they predict liver-related outcomes compared with biopsy, and how their accuracy varies in key subgroups.

“I think we should adopt it now,” Younossi said. “The data is not perfect, but it's pretty good, and these tests should be adopted in every clinical practice.”

He stresses that waiting for a flawless diagnostic tool risks further delay in addressing a disease that is already a leading cause of liver transplantation and hepatocellular carcinoma in the United States. Instead, he calls for implementation across primary care, endocrinology, diabetology, gastroenterology, and hepatology. MASLD, he notes, should be viewed similarly to other diabetes-related complications. Just as clinicians routinely screen for retinopathy and nephropathy, liver risk assessment should become standard practice in patients with metabolic disease.

At the same time, he notes that important gaps remain. While current NITs are highly effective for identifying advanced fibrosis, they are less precise in detecting patients with earlier yet clinically meaningful stage 2 (F2) fibrosis. Younossi points to ongoing work leveraging large datasets, machine learning, and artificial intelligence to develop more refined combination algorithms and calls for a paradigm shift in drug development. With NITs now guiding real-world clinical decisions, he argues that clinical trials should move away from mandatory biopsy-based enrollment and instead transition toward NIT-based designs that better reflect contemporary practice.

He also notes that barriers to adoption extend beyond diagnostics, with awareness remaining a major challenge requiring education at multiple levels: provider, public health policy, and global health leadership.

“I think in the next 5 years, you'll see additional drugs and more help for patients with progressive MASH,” Younossi said. “In that context, I think it’s going to be very important that we identify those patients, we develop care pathways where we connect these patients who are at risk with a care provider that will not only give them advice and properly manage their cardiometabolic risks with diet, exercise, and also the medication that we have available for diabetes and hypertension, but also, if they are candidates for treatment with MASH drugs, that they're offered. We'll have more drugs in the pipeline, and hopefully we'll have patients ready by then.”

Editors’ Note: Younossi reports relevant disclosures with Intercept, Cymabay, Boehringer Ingelheim, Ipsen, BMS, GSK, Novo Nordisk, Siemens, Madridgal, Merck, Aligos, Akero, Sanofi and Abbott.

Younossi ZM, de Avila L, Petta S, et al. Diagnostic Accuracy of Non-Invasive Tests for MASLD Across Age, Type 2 Diabetes, and Obesity Subgroups: A Multinational Study. 

. Published online January 28, 2026. doi:10.1016/j.cgh.2026.01.016

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Younossi emphasizes the need for NIT-based risk stratification for MASLD, citing his research supporting their widespread adoption across clinical settings.

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MASH / MASLD

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Rudolf Valenta, of the Medical University of Vienna

Seasonal Allergen Exposure Recalls IgE Plasmablasts in Birch Allergy, With Rudolf Valenta

A new longitudinal study found that IgE⁺ plasmablasts are the primary cellular drivers of seasonal IgE increases in birch pollen allergy.

, of the Medical University of Vienna, about the study’s implications. He highlighted the significance of increased seasonal IgE without a corresponding IgG response.

“Look, this is a very hot debate,” Valenta said. “There [are], I would say, two different schools here. There's one school that comes from mouse immunology. In the mouse, there is something like a sequential car switch, so if you start to sensitize a mouse to develop IgG antibodies, it's usually done by injection or by high doses of inhalation, the mouse develops IG and IgG antibodies against the same epitopes. In the human, this is not the case, because if the human would produce the IgG antibodies against the same epitopes as IgE, the person would be protected and not be allergic. The story is that [people] …push this idea of the sequential car switch in, I dare to say, very important journals here, and it's true for the mouse. The thing is, [when we] undertake our investigations in patients and in the patient, it's different.”

In this study, patients have no induction of IgG antibodies, nor are these antibodies against the IgG epitopes. However, this is the case of IgE antibodies.

If seasonal exposure triggered IgG against the same epitopes, it would act like natural immunotherapy, generating blocking IgG antibodies. Except, this does not happen; people become more sensitized after the season.

“So that's one of the reasons why we put a little bit of emphasis on this,” Valenta continued. “It’s a major observation.”

Bet v 1–specific IgE levels increased significantly during peak pollen season compared with pre-season (TP1 vs TP3; 

 < .01) and declined after the season ended (TP3 vs TP5;

 < .05). In contrast, bet v 1–specific IgG1 and IgG4 levels did not show significant seasonal changes.

Flow cytometry demonstrated a significant rise in circulating IgE⁺ plasmablasts (CD19⁺CD27⁺CD38⁺CD20low) during pollen exposure. Epitope mapping showed that the seasonal IgE boost targeted pre-existing conformational epitopes of Bet v 1, rather than generating new specificities. Functionally, this plasmablast-derived IgE reloaded effector cells, restoring allergen-specific basophil activation that had waned outside the season.

Valenta said that omalizumab could have upstream effects beyond neutralizing circulating IgE. Because the antibody does not bind IgE already attached to high- or low-affinity receptors, it may selectively target IgE-expressing B-lineage cells. This raises the possibility of weakening IgE memory responses, although clinical studies are needed.

“What we actually proposing is that this antibody could be used to eliminate such cells, and that could be a very strong bullet in killing IG responses in patients,” Valenta said. “It's different from the idea of the Regeneron [company], who want to prevent the gas switch, because this is something we think is not so important [for] the patients. We also say it's not the plasma cells, because they have a kind of continuous production that fades away, so we have in the middle what we think is a crucial cell that we can target.”

Byazrova, M., Litovkina, A., Eckl-Dorna, J. 

 Seasonal allergen exposure recalls IgE+ plasmablasts to reload allergic effector cells. 

https://doi.org/10.1007/s44466-025-00018-w

Valenta discusses how seasonal allergen exposure selectively boosts IgE production through plasmablast recall, without a coordinated IgG response.


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Seasonal Allergy

Ruchika Goel, MD, is a professor and associate vice chair of research at SIU School of Medicine.

in neonates and older children, reduced platelet increment (PI) did not lead to worse clinical outcomes, suggesting that this marker does not precipitate an increased, automatic need for transfusion.

In addition to these findings, study investigators draw attention to data that 3.6% of neonates and older children had ≥1 platelet transfusion, highlighting the importance of critically assessing transfusion practices in this population.

“From a clinical perspective, we need to assess our adherence to the platelet transfusion guidelines and also the marker, post-transfusion platelet increment. It may be an imperfect surrogate for looking at patient-centred outcomes,” said Ruchika Goel, MD, professor and associate vice chair of research at SIU School of Medicine, in an interview with 

 “For example, if you're giving platelets as prophylaxis to prevent bleeding or as therapy to treat bleeding. From a clinician's lens, this study points to judging your effectiveness by the clinical context and the overall bleeding risk, and not just by the platelet count increment or the bump alone.”

Transfusions are the only available treatment to raise platelet counts in thrombocytopenic infants, aiming to stop or prevent bleeding. While they can prevent bleeding, platelet transfusions are associated with increased inflammation and can sometimes increase mortality or morbidity in neonates.

Goel and colleagues defined a platelet transfusion event as the issue of a platelet product by the transfusion service within the encounter start and end times. They calculated transfusion incidence as a binomial proportion of encounters during which ≥1 platelet product was issued, for the total population and by patient sex, age, and self-reported race and ethnicity.

The cohort study involved data on 249,340 inpatient encounters from 7 blood centers and 22 hospitals collected by the ​​Recipient Epidemiology and Donor Evaluation Study-IV-Pediatric. The included patients were 0 to < 18 years of age. Investigators defined neonates as those < 28 days of age, and patients were otherwise considered older children.

Goel and colleagues observed ≥1 platelet transfusion in 3.6% of the study population (n = 8874). Of these, 3.3% were female, 3.7% were male, and the average age was 2.5 years, with a median weight of 1.6 kg.

Upon analysis of 40,779 platelet transfusion episodes, the median number per patient encounter was 2. 

In neonates, 32.2% of platelet transfusions were given at pretransfusion platelet counts < 25 × 103/µL, the remaining were given at increased pretransfusion platelet counts, including 38.5% at >25-50 × 103/µL, 19.6% at >50-100 × 103/µL, and 9.7% at >100 × 103/µL. The median transfusion dose was 14.9 mL/kg.

In older children, investigators analysed 26,570 transfusion events, with 19.0% of platelet transfusions given at pretransfusion platelet counts < 10 × 103/µL and the remaining were at higher pretransfusion platelet counts, including 3.0% at >100 × 103/µL. The median transfusion dose was 9.6 mL/kg.

Overall, investigators saw significantly elevated pretransfusion platelet count in neonates (34 × 103/µL [20-54 × 103/µL] compared with older patients (22 × 103/µL [11-40 × 103/µL]; 

 < .001). Post-transfusion PI was highest for pretransfusion platelet counts < 25 × 103/µL and decreased for higher counts, becoming negative (median, −25 × 103/µL for counts > 100 × 103/µL. Similarly, among infants and older children, PIs were highest for counts <10 × 103/µL and decreased for higher counts, becoming negative (median, −22 × 103/µL) for counts > 100 × 103/µL.

Platelet components stored in PAS had reduced odds of posttransfusion PI higher than 15 × 103/µL compared with platelet components not stored in PAS (adjusted Odds Ratio [AOR], 0.32 [95% CI, 0.27-0.37). Platelet storage > 3 days) was associated with decreased odds of PI > 15 × 103/µL (AOR, 0.67; 95% CI, 0.58-0.76 to 0.82; 95% CI, 0.76-0.88). Pathogen-reduced platelet components were associated with lower odds of achieving an increment higher than 15 × 103/µL (AOR, 0.82 [95% CI, 0.73-0.92]).

Assessing donor factors, investigators observed male sex was associated with reduced odds (AOR, 0.92; 95% CI, 0.86-0.98) of posttransfusion PI >15 × 103/µL per transfusion event. Additionally, donor age of ≥ 40 years compared with donor age 25 to < 40 years was independently associated with reduced odds of a PI >15 × 103/µL platelet increment (AOR, 0.79; 95% CI, 0.72-0.86).

In multivariable analysis, no donor or platelet characteristics were associated with a difference in risk of hospital discharge after 7 days (Adjusted Rates Ratio [ARR], 1.03; 95% Confidence Interval [CI], 0.89-1.20] for PR). Further, the rate of mortality was unchanged among platelet characteristics after an offset for the hospital length of stay of the encounter (ARR, 0.66 [95% CI, 0.42-1.04] for PR).

“A lower platelet increment should not automatically be used as a marker to lead to higher need for transfusion or, hence, an increased transfusion burden, because we are not necessarily seeing these to be related to clinical outcomes.”

References
Goel R, Karam O, Warden DE, et al. Platelet Transfusion Practices and Outcomes in Neonates and Children. 

https://doi.org/10.1001/jamanetworkopen.2025.54531

Neonatal Platelet Transfusions See Increased Inflammation, Not Reduced Bleeding. Hematology Advisor. Published November 25, 2025. Accessed February 12, 2026. 

https://www.hematologyadvisor.com/news/neonatal-platelet-transfusion-inflammation-bleeding-treatment-risk/

Podcasts

Low post-transfusion platelet increments did not predict mortality or length of stay in pediatric patients.

Hematology

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When Platelet Increments Matter, With Ruchika Goel, MD

Jeffrey Downey, PhD, is a postdoctoral student at the Swirski laboratory at Icahn School of Medicine at Mount Sinai.

Interferon 1 Responsible for Causing Cardiac Events During Influenza Infection

Researchers at Mount Sinai have located a cellular mechanism responsible for the correlation between 

The connection between influenza and cardiac events has long been studied, with research from 2018 determining that patients were 6 times more likely to have a heart attack in the week after receiving a flu diagnosis. Via data obtained from the Flu and Other Respiratory Viruses Research (FOREVER) cohort, investigators saw a substantial association between respiratory infections and acute myocardial infarction.

Additionally, a study from the CDC in 2020 found that cardiac events were quite common in patients hospitalized for influenza infection. After examining >80,000 patients over 8 flu seasons, investigators found that almost 12% experienced an acute cardiovascular event. Older age, tobacco use, 

, and renal disease were significantly associated with increased risk as well.

“There’s always been an appreciation that influenza is bad for the heart; if you have a large number of cardiovascular comorbidities, influenza is going to be worse,” Jeffrey Downey, PhD, a postdoctoral student at the Swirski laboratory at Icahn School of Medicine at Mount Sinai, told 

 in an exclusive interview. “But we provided mechanistic insight as to why this may be, showing that influenza has the capacity to leave lasting scars.”

Downey and colleagues investigated the autopsies of 35 hospitalized patients who died of influenza. With these data, they discovered that >85% had ≥1 significant cardiovascular comorbidity, including 

, and cardiac fibrosis. Additionally, the team uncovered the mechanism causing cardiac damage.

Briefly after infecting the lungs, the influenza virus targeted a circulating myeloid pro-dendritic cell 3 (pro-DC3), which expressed high concentrations of chemokine receptor CCR2. The heart attracts pro-DC3 due to its production of CCL2 – after entering the heart, the virus leaves pro-DC3 and infects cardiomyocytes to trigger production of type 1 interferon (IFN-1). In turn, IFN-1 receptors engaging with cardiomyocytes cause tissue damage and compromise heart function.

Based on mouse models, the team developed a hypothetical treatment involving the dampening of IFN-1 receptors exclusively in cardiomyocytes. This protected the heart and preserved anti-viral immunity in the lung. Downey and colleagues hypothesized that a systemic delivery of modified RNA therapy to the heart’s muscle cells would modulate the IFN-1 signaling pathway.

Although this study is purely hypothesis-generating, and actual attempts at treatment are far in the future, Downey and colleagues are actively researching the use of a safe and effective systemic delivery method of this modified RNA therapeutic directly into the heart’s muscle cells rather than a direct injection used in the proof-of-concept study introducing the mod-RNA pathway. Additionally, further investigation is being conducted into pro-DC3 itself, aiming to determine the reason for its susceptibility to influenza and whether this is mirrored across other infections like SARS or COVID-19.

“Moving forward, something we should always be paying attention to is that getting through influenza may not be the only goal,” Downey said. “The main thing we should be focusing on is still prevention and mitigation of infection, but in those with high risk, we should potentially be looking at some immunotherapies that can dampen immunological pathways activated specifically in the heart.”

Editor’s Note: Downey reports no relevant disclosures.

Mount Sinai Hospital. Mount Sinai scientists uncover link between influenza and heart disease. 

. February 9, 2026. Accessed February 12, 2026. 

https://www.eurekalert.org/news-releases/1115515

Kwong JC, Schwartz KL, Campitelli MA, et al. Acute myocardial infarction after laboratory-confirmed influenza infection. New England Journal of Medicine. 2018;378(4):345-353. 

Chow EJ, Rolfes MA, O’Halloran A, et al. Acute cardiovascular events associated with influenza in hospitalized adults. Annals of Internal Medicine. 2020;173(8):605-613. 

Downey J, Oliveira-Coelho A, Kiss MG, et al. Influenza hijacks myeloid cells to inflict type-I interferon-fueled damage in the heart. Immunity. Published online February 9, 2026. 

Downey discusses the recent discovery of influenza’s interaction with the interferon 1 pathway, as well as a hypothetical method for preventing it.

Cardiology

Cardiology condition center page is a comprehensive resource for clinical news and insights on cardiovascular and cardiometabolic diseases. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for heart disease and cardiovascular events, as well as associated diabetes, renal failure, and more...

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Interferon 1 Responsible for Causing Cardiac Events During Influenza Infection, With Jeffrey Downey, PhD

vice president of programs, public affairs, and research at Lung Health Foundation.

New Lung Cancer Risk Calculator Streamlines Screening Eligibility, With Jessica Moffatt, PhD

The Lung Health Foundation has introduced a simplified 

 calculator designed to help patients and clinicians better understand eligibility for organized screening programs across Canada. Built on the validated PLCOm2012 risk prediction model, the online tool translates a previously spreadsheet-based calculator into a plain-language, 10-question interface that generates a 6-year lung cancer risk estimate in 2 – 3 minutes.

Lung cancer screening differs from other cancer screening programs in that it is risk-based rather than population-based. Patients must meet age criteria and have a sufficient smoking history before undergoing a formal risk assessment through a provincial program. That multi-step structure can create uncertainty in primary care settings, particularly during time-limited visits.

, investigator Jessica Moffatt, PhD, vice president of programs, public affairs, and research at Lung Health Foundation, emphasized that the calculator does not diagnose cancer and does not determine formal screening eligibility.

“The only official risk assessment result is the risk assessment result that's conducted with the screening program,” Moffatt said. “What this can do is this can be supplemental to that clinician-patient conversation to really help facilitate that informed decision-making process between the clinician and the patient to help the clinician understand, should I make the referral for screening? Once that referral is made, the official risk assessment is conducted. This is just a tool to help the clinician understand, is my patient actually eligible, or may they be eligible for lung cancer screening?”

The calculator produces a downloadable PDF summary without jargon, allowing patients to bring their responses into an appointment. Developers said this feature was designed with primary care workflows in mind, enabling clinicians to review key inputs, such as age, smoking exposure, comorbidities, and prior cancer history, without navigating a complex risk model during the visit.

The tool may also benefit individuals without a regular primary care provider. In some provinces, patients can self-refer to lung cancer screening programs. A preliminary risk estimate may help them decide whether contacting a screening site is warranted.

The PLCOm2012 model is structured to balance benefit and harm. Low-dose CT screening carries risks, including false positives and downstream procedures. By anchoring the calculator in an established risk framework, the Lung Health Foundation aims to support appropriate screening conversations while reinforcing that patients with symptoms, such as persistent cough, hemoptysis, or unexplained weight loss, require diagnostic evaluation rather than screening.

With many lung cancers still diagnosed at advanced stages, the Lung Health Foundation positions the calculator as an entry point to informed discussions, not a substitute for clinical judgment.

“We recognize how busy primary care providers are, and this is a tool that can help primary care providers, in a very streamlined way, have that discussion with their patient that lung cancer screening may be right for them,” Moffatt said. “It's convenient for the public, but it's also convenient for clinicians.”

‘Think Mortgage Calculator, But for Lung Cancer Risk’: A More User-Friendly Self-Serve Tool Gives Canadians and Healthcare Providers a Clearer Starting Point. GlobeNewswire. Published on February 4, 2026. Accessed on February 12, 2026. 

https://finance.yahoo.com/news/think-mortgage-calculator-lung-cancer-123000493.html?guccounter=1&guce_referrer=aHR0cHM6Ly9zdGF0aWNzLnRlYW1zLmNkbi5vZmZpY2UubmV0Lw&guce_referrer_sig=AQAAANFnUl3Oz4FMn8kNg43vqehf_7SF1nUmh0k1LLaCpbMdC9_T-6vswljrh6fwLmRxxEGMwz-0dnFQjGKKfqJJWi0oQETyZDsfkBeYGnzfUqTpyxdDpQumjFy3NQ7FXywWocCd8t8GXlRUV3iH2g3ONrsSgg6yIeNYhnHt2F9RSZuO

The free, user-friendly calculator provides a 6-year lung cancer risk estimate to help patients and clinicians assess screening eligibility.


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Tool Predicts a 6-Year-Risk Lung Cancer Risk in Minutes, With Jessica Moffatt, PhD

Abigail Brooks is an assistant managing editor for 

She joined MJH Life Sciences in August 2023 shortly after graduating from Monmouth University where she earned her BA in Communication with a concentration in Public Relations/Journalism and later an MA in Interactive Digital Media. She enjoys traveling, running, and reading books. She can be reached at abrooks@mjhlifesciences.com.

Articles

Survey findings highlight abdominal and bowel symptom control, affordability, and formulary or insurance coverage as factors driving perceptions and prescribing patterns of PERT.

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Real-World Prescribing Patterns of PERT in Exocrine Pancreatic Insufficiency

Mark Kaufmann, MD, is a clinical professor in the Department of Dermatology at the Icahn School of Medicine at Mount Sinai in New York City.

Mark Kaufmann, MD, speaks on maximizing your billing effectiveness in the era of dwindling reimbursements and ICD-10.

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Strategies on Maximizing Billing Effectiveness for Clinicians, With Mark Kaufmann, MD

Younossi explains the growing interest in NITs for MASLD and reviews his research on their performance in age, diabetes, and obesity subgroups.

Diagnostic Performance of NITs Across MASLD Subgroups, With Zobair Younossi, MD, MPH

Frank Gonzalez is an attending physician at Children’s Hospital Los Angeles and an assistant professor of clinical pediatrics at Keck School of Medicine of USC.

Gonzalez explains how new findings in weather-related emergency department visits and pain in pediatric sickle cell disease can guide clinicians. 


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Managing Climate Change-Induced Sickle Cell Pain Crises With Frank Gonzalez, MD

David Rizik, MD, is an interventional cardiologist at Banner University Health.

Rizik and Morris discuss the Heartflow PCI Navigator, which analyzes CT scans to generate 3D models of calcium blockages ahead of procedures.

Banner Health Debuts AI 3D Vascular Modeling Device, With David Rizik, MD, and Michael Morris, MD

Chelsie Derman is an associate editor for 

who covers psychiatry, sleep medicine, geriatrics, migraine, and allergy. She joined MJH Life Sciences in September 2023 after graduating from The College of New Jersey with a bachelor’s degree in journalism and professional writing. In her free time, she enjoys creative writing and reading.

In this Q&A, investigators Maria Byazrova and Rudolf Valenta discuss findings on plasmablast's role in seasonal IgE surge when it comes to birch allergy.

Seasonal IgE Surge in Birch Allergy Driven by IgE⁺ Plasmablasts: Q&A With Investigators

The data represent the highest and most significant improvement in AHV and the first statistically significant improvement in body proportionality in achondroplasia.

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Oral Infigratinib Meets Annualized Height Velocity Endpoint in Phase 3 Achondroplasia Trial

Ashfaq Marghoob, MD, is a dermatologist specializing in the diagnosis and treatment of cancers of the skin and the director of the Memorial Sloan-Kettering regional skin cancer clinic.

In this Q&A segment of his interview, Marghoob speaks on-site at Maui Derm on tips related to dermoscopy and skin cancer detection.

Discussing Pediatric Dermoscopy and AI for Skin Cancer Detection, With Ashfaq Marghoob, MD

Desai discusses his recent observational cohort study indicating finerenone’s substantial reduction of heart failure exacerbation risk in patients with HFpEF.

Heart Failure

The HCPLive heart failure page is a resource for medical news and expert insights on HF. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for heart disease, reduced and preserved ejection fraction, and more.

Finerenone Outperforms Spironolactone for Heart Failure Exacerbation in HFpEF, With Nihar Desai, MD, MPH

Alex Hillenbrand is an assistant editor for 

. She earned her BA in English from Lafayette College in 2023 and went on to write for pop culture, entertainment, and sports media outlets before joining MJH Life Sciences in 2025. In her free time, Alex enjoys cooking, going on walks, and meeting new people. Contact her at mjhlifesciences.com.

The American Society of Hematology released new 2026 Guidelines for Management of Relapsed/Refractory ALL in AYAs, discussing immunotherapy and personalized decision making. 


Latest News

From Validation to Implementation: Scaling NITs in MASLD Care, With Zobair Younossi, MD, MPH

Seasonal Allergen Exposure Recalls IgE Plasmablasts in Birch Allergy, With Rudolf Valenta

When Platelet Increments Matter, With Ruchika Goel, MD

Interferon 1 Responsible for Causing Cardiac Events During Influenza Infection, With Jeffrey Downey, PhD

Tool Predicts a 6-Year-Risk Lung Cancer Risk in Minutes, With Jessica Moffatt, PhD