Even though the role of prolactin in psoriasis is not completely clear [17,18], recent studies suggest that it may enhance IFN-gamma-induced CXCL9, CXCL10, and CXCL11 production in keratinocytes via activation of STAT1, NF-kappaB, and IRF-1 through the JAK2 and MEK/ERK pathways and thus may promote type 1 T-cell infiltration into psoriatic lesions [19]. The gene discussed is JAK2; the disease is psoriasis.