Our ever-expanding knowledge of the pathogenesis of psoriasis has finally matched that of other genetically based autoimmune diseases. No longer simply considered a disease of the skin, psoriasis is now widely recognized as a hereditary-based, systemic disease with cutaneous manifestations. The pathogenesis of psoriasis involves both genetic predisposition and T cell-dependent mechanisms. Population, family, and twin studies all strongly suggest an important genetic component, coupled with an environmental trigger, in the pathogenesis of psoriasis. Furthermore, genetic-linkage studies have found multiple genetic loci for psoriasis. The autoimmune component of psoriasis is substantiated by multiple findings, including the isolation of activated T cells within the lesions. Our current therapies for psoriasis are not target-specific. As we further unravel the genetic basis for psoriasis, treatments will improve together with the exciting potential for gene therapy in the future.