There is broad consensus that a mixed interleukin (IL)-17 (T helper type 17: Th17) and interferon gamma (IFNγ)/tumour necrosis factor (TNF) response (Th1/Tc1), driven by a vast network of cells, such as T and dendritic cells, plays a dominant role in promoting keratinocyte hyperproliferation and aberrant differentiation in psoriasis (10–12). This evidence concerns the gene IFNG and psoriasis.