HIF-1α has been shown to activate different molecules to achieve this goal, including activation of anti-apoptosis genes in tumor cells, activation of PD-L1 to escape CTL-mediated killing, activation of CD39/CD73 to accumulate adenosine and inhibit CTL, induction of autophagy to inhibit NK cell mediated lysis, activation of CD47 to block phagocytosis by macrophage, and induction of chemokines/cytokines to recruit T regulatory cells (Tregs) and marrow derived stem cells (MDSCs) to inhibit tumor immunity [7, 8]. This evidence concerns the gene ENTPD1 and neoplasm.