When TNF-α is significantly inhibited, the balance between TNF-α and IFN-γ is destroyed, thereby causing an increase in the production of IFN-γ by dermal plasmacytoma dendritic cell and excessively facilitating the migration of cluster of differentiation 8 + t cells to the epidermis; as a result, dendritic cell cells are activated and maturated, thereby inducing the autoimmune response.[30,36] The interleukin (IL)-23/T-helper (Th)-17 axis is also vital to the pathogenesis of TNF-α-antagonist-induced psoriasis. This evidence concerns the gene IFNG and plasmacytoma.