Since IL-23 from tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthetase (iNOS)-producing dendritic cells (TIP-DCs) is required for maintaining IL-17-producing cells through an autocrine mechanism via TNF-α, the role of these cytokine networks in psoriasis pathogenesis have been shown by the therapeutic effectiveness of cytokine-blocking biologics. This evidence concerns the gene IL23A and psoriasis.