IL-12 is well known as a classic mediator of antitumor immunity, mainly attributed to its capacity to promote Th1 cell and CD8+ T cell differentiation and NK cell activation and, subsequently, to enhance IFNγ secretion, which is required for the efficient presentation of tumor antigens, T cell recruitment to the tumor site, and the intratumoral survival and expansion of cytolytic effector T cells [103,104,105,106,107,108]. This evidence concerns the gene CD8A and neoplasm.