Psoriasis is considered to be a T cell-mediated disease, whereby a mix of Th1 and Th17 T cell-derived cytokines, such as IFNγ, IL17A and IL22, drive the pathological hyperproliferation, aberrant differentiation and the autoimmune amplification of keratinocytes that ultimately drive psoriatic plaque formation. Here, IFNG is linked to psoriasis.