Besides arginase and iNOS, tumor-induced MDSCs might overexpress HIF-1α, STAT3, C/EBPβ [23], [29], BCL-2 and VEGFR1 signalling molecules [25], [36] but little is known about the involvement of the inhibitory co-stimulatory molecules PDL1 and CTLA4, important factors contributing to tumor-mediated immune suppression [37]–[43], which blockade by monoclonal antibodies represents an emerging anti-cancer strategy [16], [44], [45]. The gene discussed is CTLA4; the disease is neoplasm.