The genetics of psoriasis are interesting from a number of different angles. First, some of the genes linked to inflammatory diseases such as psoriasis, inflammatory bowel disease, and rheumatoid arthritis are shared across all 3. Although there may be different triggers, there also may be commonalities among these diseases. So, it might be the case that some patients with psoriasis, for instance, are already on the road to developing inflammatory bowel disease at some point in time. 

The genetic studies also show us that psoriasis is an incredibly complex disease. One person’s psoriasis is not the same as the next person’s psoriasis. A 2017 meta-analysis by Tsoi et al had an effective sample size of approximately 40,000 patients with psoriasis and analyzed approximately 9 million markers. Some 63 loci linked to psoriasis were estimated to account for only about 28% of the genetic heritability of psoriasis, so the current understanding is incomplete. However, it is interesting to see that links between psoriasis and mutations in interleukin-23 (IL-23)–related genes were again found, including in genes for the IL-23 receptor. IL-23 is a crucial proinflammatory cytokine in autoimmunity and specifically in psoriasis. 

From the perspective of personalized therapy, genetic assays are not yet able to answer the question of who will become a long-term responder to any particular biologic therapy. Alefacept was actually the first biologic that was approved by the US Food and Drug Administration for moderate to severe psoriasis. And, at the time of its introduction, clinicians were eager for a test that would identify patients who would respond to this drug because it worked well in only a small subset of patients. In contrast, today we have a number of highly effective biologic therapies, including those that inhibit tumor necrosis factor, IL-17, and IL-23, and we can effectively treat the vast majority of patients within just a few months. So, I am fairly confident that when I start a patient on 1 of these therapies, it is going to work very well, and I do not need a predictive test. If a particular therapy does not work well, or it stops working, it might be because the patient has developed an antibody to the drug. I am not aware of any genetic assays that would tell me who is going to develop antidrug antibodies (or who may be nonadherent to the treatment). 

Still, even today, we can effectively personalize treatment. To me, an important aspect of personalization relates to educating patients about their disease so that they can be engaged in their treatment and be familiar with the available treatment options. You might explain the mechanism in more relatable terms, drawing parallels with natural processes. I am a data-driven clinician, but I also appreciate that anecdotes can be quite helpful to patients. For instance, you can say to the patient, “I think that this particular agent is a really good choice for you because I had another patient whose psoriasis was a lot like yours and they did really well on this.” You also personalize based on patient preferences, including preferences regarding route and dosing frequency. And, when trying to educate patients about their disease and their treatment options, I like to encourage them to join the National Psoriasis Foundation and to make use of the many educational resources that it provides.