The uncontrolled tumour growth and TME remodelling prevents the immune system to control the tumour progression and favours the recruitment of CD4+ T regulatory (Tregs) cells, which supress the priming, activation and cytotoxic activity of effector immune cells, such as Th1 cells, CTL, macrophages, NK cells, and neutrophils, through contact-dependent (PDL-1, LAG-3, CD39/73, CTLA4, or PD1) and contact-independent mechanisms (secretion of IL-10, TGF-β, prostaglandin E2, adenosine, and galectin-1, among others) [122]. This evidence concerns the gene ENTPD1 and neoplasm.