Tregs influence tumor growth by acting either on supporting the survival of cancer cells through the secretion of growth factors or via the inhibition of immune cell effector functions through multiple mechanisms, including the expression of IL-10, TGF-β, CTLA-4, and granzyme B. On the one hand, cancer cell-derived IL-1α induces the recruitment of Tregs to foster the formation of an immunosuppressive situation by increasing CCL22 expression. This evidence concerns the gene CTLA4 and cancer.