Within this paradigm, the principal interpretation of the high levels of clinical improvement of psoriasis in response to treatment with ustekinumab (which targets the p40 molecule shared by IL-12 and IL-23), as well as of the emerging data indicating even higher response rates for antibodies against IL-17A (blocking IL-17A homodimers and IL-17A/F heterodimers) and IL-17 receptor A (potentially blocking IL-17A, IL-17AF, IL-17F, IL-17C and IL-17E), has been that these therapies antagonize major effector cytokines related to the IL-23/Th17 axis 18. This evidence concerns the gene IL17A and psoriasis.