Thus, IFN-γ and IL-22 inflammatory cytokines are deeply involved in the pathogenesis of psoriasis, and their Janus Kinase (JAK)1/JAK2/signal transducers and activators of transcription (STAT)1 and JAK1/tyrosin kinase (TYK)2/STAT3 proximal signaling are aberrantly activated, as highlighted by STAT1 and STAT3 signatures in psoriatic skin lesions [7–10]. This evidence concerns the gene IFNG and psoriasis.