Moreover, it is well accepted that Th1-derived IFN-γ, in interaction with IFN-α and TNF, is a key cytokine in the pathogenesis of psoriasis and is further described to stimulate DDC to produce IL-1 cytokines and IL-23, both critical mediators of Th17 polarization, the major subset in chronic psoriatic plaques [33, 136–138]. The gene discussed is IL1B; the disease is psoriasis.