Jason Hawkes, MD, MS

Expanding biologic options are advancing precision medicine in atopic dermatitis.

Targeted therapies are helping clinicians better understand disease heterogeneity and inflammatory pathways.

Comparing treatment responses may improve personalized therapy selection for patients with atopic dermatitis.

As the dramatic expansion of the treatment landscape for 

 has continued in recent years, more and more targeted biologics and small-molecule medications have been providing clinicians with additional options in the armamentarium for patients with eczema.

Beyond broadening the therapeutic armamentarium, such advances in the atopic dermatitis space are also providing new insights into the underlying biology of the inflammatory skin disease, helping researchers better comprehend why patients respond differently to various drugs. In his on-site interview with 

Revolutionizing Atopic Dermatitis (RAD) Conference

 in Nashville, Tennessee, Jason Hawkes, MD, professor of dermatology at the University of California, Davis, touched on the ways in which the growing number of available therapies are shaping the future of precision medicine in dermatology.

In the following written Q&A interview, Hawkes explains why clinicians are learning more than ever about the distinctions between inflammatory pathways, about disease heterogeneity, and about the ways in which these discoveries may eventually lead to more personalized care:

You gave a session at RAD titled ‘Connecting AD to Other Dermatologic Disorders and Related Comorbidities.’ Why did you feel it was important to highlight the elements from your portion of this talk for dermatologists?

Historically, we had type 2 inflammation, but we had really a single product in atopic dermatitis. Then we started dissecting out the layers. We had the first therapy, obviously, blocking one receptor, blocking multiple cytokines. Then we started seeing the development of new therapies where we're blocking just a single cytokine with IL-13. We then had IL-31 receptor, but then we kind of went backwards a little bit in terms of blockade, with the JAK inhibitors being a little less specific, more selective for a particular enzyme, but hitting multiple pathways.

What that's allowed us to do is then compare and contrast responses. Why do some people respond to these therapies for atopic dermatitis, but only certain therapies work in urticaria or nasal polyps, for example? We're just now scratching that surface. Initially, we weren't sure what other pathways were coming, but now that we have these individual products, we can start to see the pros and cons of each of them. They're all going to have a place. We are now testing in humans, rather than in cell cultures or mouse models; we're seeing the benefits. We're seeing the drawbacks of different products, and that's allowing us to get closer to personalized medicine, where we can start to tailor the therapies to the patient in front of us. That's important.

For those then who weren't able to attend this session, what would you say were the biggest takeaways you hope clinicians will walk away with regarding atopic dermatitis treatments?

I think we've started to see the differentiation, where we're seeing this unique role for IL-4 in picking up some of the differentiation of the T cells, some of these autoantibodies, playing a role in unique diseases that we wouldn't necessarily have thought type 2 would have played a role. Things like chronic spontaneous urticaria and bullous pemphigoid. On the other spectrum, we have really an itch-centric therapy with blockade of the IL-31 receptor, and then we're seeing within the IL-13 space really this development of expertise in controlling atopic inflammation. We're seeing the benefits of extended dosing with these therapies that do a really good job at shutting down IL-13 in the tissues.

This has really been kind of helping us understand, again, where do we put these different products? Also, what are they teaching us? When we have a patient who initially responds and then stops responding, what does that mean? What happens if someone's inflammation gets better, but their itch persists, or vice versa? We hit their itch, and you see different changes. I think this has given us a chance to really explore this heterogeneous group. We've talked about atopic dermatitis, but there are probably these subsets within that bucket. Now we're starting to tease them out, and it's giving clinicians insight into what they saw in the clinic, which is this heterogeneity. I think it's going to help us eventually find the best treatment for the right patients.

How close are we in the dermatology space to a new era of personalized medicine?

 I think when we talk to patients, you hear these patients talk about type 2 inflammation. They're not saying those words, but they're saying, ‘I grew up, and I developed allergies as a kid, and I had exercise-induced asthma,’ and then ‘In college I started developing this rash and the flexural.’ They're telling you a story, and I think for a lot of clinicians that's natural to say, ‘I'm hearing this flavor of type 2 inflammation.’ In our urticaria patients, they start talking about [someone having] celiac disease, and say, ‘I develop hypothyroidism and have multiple food or drug allergies.’ So we start to hear those stories. I don't think we knew what to do with that information.

We just kind of categorize these patients as being, you know, atopics. We say that all the time. We're having atopy, and I think that that's been an evolution for us to kind of start to hear that story. But now we can start to attach it, you know, to particular therapies, and that's advancing care. The issue has been the system as really applying a one-size-fits-all, or you think about the prior authorization process where it's a formulary has been selected maybe based on cost that you know you have to go through this drug that's you know inexpensive or you know we've decided that this therapy's first line before you can get to the second or third line option, and those are counterintuitive because that one size fits all is the antithesis of personalized medicine.

To have an insurance company or a healthcare system say, ‘You have to use this drug’ really takes away the ability for the doctor to say, ‘I'm hearing this story.’ And I think they're actually going to do better on this type of therapy. But you may not be able to access it. I think we're fortunate in the US, where we have copay programs and samples, and we have access as a community to get medications that we think are the right fit. But we really haven't had a lot of science backing up why I choose therapy A, but my colleague might choose therapy B, or someone else might choose therapy C. We need some metrics or measures or testing that can help us better select therapies at the outset that have a higher likelihood of working because we just want to get those patients better. We're in a try-and-fail system, and we don't always know they can look like they're going to respond and not respond.

It seems a lot of what clinicians hate about prior authorization is about misaligned incentives and how it prevents patients from getting the right drug. What are your thoughts on prior authorization?

Yeah, here there's an article that's years old now, but still is relevant, which shows that when you look at the burden of prior authorizations, it's had a disproportionate impact on dermatologists. That was a paper that came out of the University of Utah. It was a well-done paper that highlights the issue, which is that across all of medicine, prior authorizations are creating an administrative burden. They don't bring in revenue for practices, but they take a lot of time. I think dermatologists have we're fortunate to have a lot of these targeted, selective therapies, but they're expensive. So how do we contain costs? Also, [how do we] not make this burden really affect those practices or trying to help patients?

I think there's a fair balance, but it's often used as a stall tactic as well. It's really hard to want to put a patient on, say, methotrexate, knowing that it's a very inexpensive medication. Knowing the drawbacks and limitations of using these therapies long term. Knowing these patients have chronic conditions. I see the rationale behind having some system in place to not be a free-for-all, but I think it has ultimately restricted the personalized care that experts can offer these that really have the expertise…We would like to really have some research and data guiding some of those decisions. I think that process has started in the research area to try to get us closer to making those better-informed decisions.

We know you discuss comorbidities of diseases such as atopic dermatitis. What comorbid conditions do you believe are still underrecognized in clinical practice?

Urticaria has been a really fun area to work in. It's probably more common. We in dermatology don't see it as much because a lot of the allergists have managed urticaria for a lot of years. But when you start to talk to people, almost every day, we talk to individuals saying, ‘I had a bout of urticaria.’ Literally at this meeting, I talked to somebody who was saying, ‘I grew up and had many bouts of urticaria,’ so we know that that's probably a little bit more common. These patients with chronic urticaria often end up suffering in silence, and they're trying over-the-counter medications. They're trying to look at what the causes might be.

I think we saw that with atopic dermatitis as well. I think that's a condition still within atopic dermatitis. I still think there are a lot more patients out there that have it. We see a small proportion of patients as a specialty. There's been a lot of data that these patients are out there in primary care or with their general practitioners that haven't been formally diagnosed. HS is another condition where we see a lot of underdiagnosis. But I think in the type 2 conditions, urticaria comes up. I think asthma is often underrecognized, especially for those that maybe have very mild asthma. Allergic rhinitis, we know, is very common. I think that's been, you know, appreciated. And when you start talking to patients, you hear that story.

What emerging research or unanswered questions related to atopic dermatitis are you most looking forward to learning more about?

One area I mentioned, sort of in in our in our panel, is how do we induce remission? One really interesting component for patients living with atopic dermatitis is that there's a subset of patients who just grow out of their disease. We don't really understand that process, and that's a really important mechanism to try to understand. We see that in other disease states, so guttate psoriasis, for example, one of those acute eruptive forms of psoriasis. But we know those patients have a risk of developing chronic plaque psoriasis. But most of them are self-limiting. So, what is it that's different in gut-based psoriasis than chronic plaque psoriasis? What's different in these patients that outgrow their disease as opposed to those that have persistent disease well into adulthood?

I think if we could uncover some of those mechanisms, what's the immune system doing? Maybe it's genetic. What's happening to corral that immune response to, you know, shut it off, regulate it, so that we don't have this, you know, persistent, chronic, active disease. That's an area where it's the silver bullet. We're all looking for ways to turn off disease, but I think that's really important for these chronic conditions. These patients want to stop living with their disease. They don't want to be on therapies, and I think obviously that move towards a cure, right, or remission, finding ways to really put disease in remission.

Disclosures: Hawkes has served as a consultant, advisory board member, investigator, and speaker for multiple pharmaceutical companies involved in dermatology, including AbbVie, Arcutis, Blueprint Medicines, Eli Lilly, Galderma, Incyte, Janssen, LEO Pharma, Novartis, Regeneron, Sanofi, Sun Pharma, Takeda, and UCB, among others. He has also received research funding and reports stock ownership in Regeneron.

Hawkes J, Lieberman J. Session 2: Connecting AD to Other Dermatologic Disorders and Related Comorbidities. Session presented at: 2026 Revolutionizing Atopic Dermatitis Conference; June 17-19, 2026; Nashville, TN.

Hawkes J. How Are New Biologics Changing Atopic Dermatitis Treatment? HCPLive. July 22, 2026. Accessed July 24, 2026. 

https://www.hcplive.com/view/how-new-biologics-changing-atopic-dermatitis-treatment-

Articles

Rapid proliferation of targeted biologics and small molecules for atopic dermatitis is enabling in vivo dissection of type 2–skewed inflammatory circuitry and clinically meaningful endotyping. Differential blockade of IL-4/IL-13, IL-31R, and broader pathway modulation with JAK inhibitors is clarifying why cutaneous inflammation, pruritus, and comorbidity signals decouple across patients. Clinical narratives of atopy and autoimmunity are increasingly actionable but remain constrained by step-therapy and prior-authorization burdens. Key research priorities include biomarkers for upfront selection and mechanisms driving durable remission.

Jason Hawkes, MD, explains how new biologics and targeted therapies are advancing precision medicine and improving personalized care in atopic dermatitis.

Q&A: How Is Precision Medicine Changing Atopic Dermatitis Care? With Jason Hawkes, MD

Personalized medicine is expanding, but prior authorization remains a major obstacle.

Earlier recognition of type 2 inflammatory diseases could improve patient outcomes.

Understanding spontaneous remission may help shape future atopic dermatitis therapies.

 care is increasingly shifting toward a more personalized treatment paradigm, but several key barriers remain before those treating patients in dermatology can consistently match individuals with the medications most likely to benefit them, according to Jason Hawkes, MD, of the University of California, Davis.

, spoke about takeaways from his session, wherein he discussed the promise of precision medicine, the challenges posed by prior authorization, and data-related questions he believes will shape the next generation of eczema care.

Prior Authorization, Precision Medicine, and Eczema Remission, With Jason Hawkes, MD

How Personalized Medicine Is Changing Atopic Dermatitis Care

Hawkes explained that clinicians have long recognized recurring clinical patterns among patients with type 2 inflammatory disease, even before today's expanding medication landscape. Histories of childhood allergy, asthma, allergic rhinitis, and eczema often point toward shared inflammatory pathways. He described newer targeted therapies as allowing clinicians to better connect these characteristics with specific approaches to therapy.

Despite this progress, he noted that the healthcare system has not fully embraced individualized treatment. Step therapy requirements and prior authorization policies often require clinicians to prescribe medications based on formulary restrictions rather than selecting therapies they believe best fit a patient's clinical profile.

Hawkes suggested that while cost containment remains important, these policies can limit physicians' ability to practice personalized medicine and delay effective treatment for patients with chronic inflammatory skin diseases. He added that future research should focus on developing biomarkers or other objective measures that help clinicians identify the therapies most likely to succeed before treatment begins.

Why Earlier Recognition of Type 2 Diseases Remains Important

Hawkes also highlighted conditions he believes remain underrecognized despite increasing awareness. He pointed to chronic urticaria, mild asthma, hidradenitis suppurativa (HS), and atopic dermatitis itself, noting many patients continue to go undiagnosed or remain managed exclusively in primary care settings before reaching specialists. Earlier recognition of these interconnected type 2 inflammatory diseases could improve access to appropriate therapies as well as comprehensive care.

What Researchers Still Learn About Atopic Dermatitis

Looking ahead, Hawkes identified disease remission as one of the field's most important unanswered questions. He noted that some individuals naturally outgrow atopic dermatitis while others experience persistent disease into adulthood, yet the mechanisms underlying this difference remain poorly understood. Determining how the immune system achieves spontaneous remission could ultimately inform strategies aimed not only at controlling symptoms but also at inducing long-term remission or even preventing chronic disease altogether.

Hawkes J. How Are New Biologics Changing Atopic Dermatitis Treatment? HCPLive. July 22, 2026. 

https://www.hcplive.com/view/how-new-biologics-changing-atopic-dermatitis-treatment

Videos

Jason Hawkes, MD, highlights issues related to prior authorization as well as raising awareness of chronic urticaria, HS, atopic dermatitis, and other diseases.

, Jason Hawkes, MD, associate professor of Dermatology at the University of California Davis in Sacramento, reflected on the evolution of 

 treatment, noted clinicians initially had only 1 single targeted biologic available for those with type 2 inflammation.

New targeted therapies are helping clinicians better understand atopic dermatitis biology.

Different inflammatory pathways may explain why patients respond differently to treatment.

Advances in precision medicine could improve individualized therapy selection for patients with atopic dermatitis.

Since then, however, Hawkes described the therapeutic landscape as having broadened notably, with the introduction of increasingly selective biologics targeting individual cytokines such as interleukin (IL)-13 and IL-31, alongside Janus kinase (JAK) inhibitors impacting multiple inflammatory pathways. He discussed these in his session at the 

2026 Revolutionizing Atopic Dermatitis (RAD) Conference

 and highlighted them in this on-site interview.

How Are New Biologics Changing Atopic Dermatitis Treatment?

According to Hawkes, this notable increase in the diversity of treatment mechanisms has allowed dermatology clinicians to have new and valuable opportunities to compare therapeutic responses across patients and disease states.

How Targeted Therapies Are Revealing Differences Between Patients

He described such advances as having extended beyond simply expanding treatment choices. As more targeted drugs have entered clinical practice, researchers have gained greater insight into why certain inflammatory pathways appear to drive some diseases but not others. Comparing responses among individuals living with atopic dermatitis, chronic spontaneous urticaria (CSU), nasal polyps, and other type 2 inflammatory disorders has begun to reveal meaningful biologic differences that were previously difficult to appreciate.

Hawkes emphasized that clinicians are now witnessing these distinctions in real-world patient care rather than relying solely on laboratory or animal models. Observing which patients respond to specific cytokine blockade, as well as identifying situations in which treatment improves inflammation without fully addressing itch, or vice versa, is helping investigators better characterize the heterogeneous nature of atopic dermatitis.

Why Personalized Medicine May Represent the Future of Atopic Dermatitis Care

Rather than viewing atopic dermatitis as a single disease entity, Hawkes suggested the condition is increasingly being understood as a collection of biologically distinct subgroups. The expanding therapeutic armamentarium is allowing clinicians to identify these differences while generating new insights into disease mechanisms and treatment response.

Ultimately, Hawkes described this shift as an important step toward precision medicine in dermatology. By continuing to define the unique inflammatory pathways driving disease in individual patients, clinicians may eventually be able to better match therapies to specific disease phenotypes, improving outcomes while further refining the management of atopic dermatitis and related inflammatory conditions.

Hawkes J, Lieberman J. Session 2: Connecting AD to Other Dermatologic Disorders and Related Comorbidities. Session presented at: 2026 Revolutionizing Atopic Dermatitis Conference; June 17-19, 2026; Nashville, TN.


Jason Hawkes, MD, explains how targeted therapies are advancing precision medicine and reshaping personalized care for atopic dermatitis.

Personalization of CSU Care With Advanced Therapies

Jason Hawkes, MD, MS, a board-certified dermatologist and associate professor of Dermatology at the University of California Davis, predicts that the management of CSU—and other inflammatory skin conditions—will increasingly incorporate precision medicine principles, powered by the expansion of targeted drug options. He posits that as more data emerge, clinicians will be able to identify disease subsets and tailor interventions based on differential responses to therapies targeting specific pathogenic mechanisms.

While the classic stepwise approach (escalating from antihistamines to targeted therapies) will likely persist for reasons of efficiency and stewardship, the growing variety of advanced treatments will permit greater flexibility and customization, particularly for patients with unique clinical characteristics or comorbidities. Hawkes stresses that this trend is visible in conditions such as psoriasis, eczema, and hidradenitis suppurativa, as well as CSU.

He also highlights the importance of ongoing research into new drug classes, such as C-kit inhibitors, and the real-world adaptation of step-up and step-down approaches based on patient response and tolerability. Hawkes concludes that the future of CSU therapy lies in weaving evidence-based pathways with the nuanced understanding of patient subtypes and evolving mechanistic insights.

Jason Hawkes, MD, MS, envisions the future of CSU management, highlighting the integration of precision medicine and targeted therapies to individualize care.


