Notably, the pathogenesis of psoriasis is considerably mediated by T helper (Th) type 1 activation and Th17 immune responses and the consequent overproduction of cytokines (e.g., Tumor necrosis factor-α TNF-α, IL-23, and IL-17) that ultimately generate a systemic proinflammatory environment. The gene discussed is TNF; the disease is psoriasis.