This cytokine profile is in agreement with PIDs affecting IFN-γ receptor or STAT4 that predispose for KS, with a KS tumor microenvironment in which PBMCs secrete high levels of Th1 cytokines, and also with KSHV encoded viral homologues of cellular chemokines, such as vMIPI-III, which counteract Th1 responses by rather skewing into a more Th2-like microenvironment for immune evasion [146,186,187,188,189,190]. The gene discussed is STAT4; the disease is Kaposi's sarcoma.