This is demonstrated by our in vivo studies in the AOM-DSS murine model of CAC, where GPR15 deficiency resulted in a significant reduction of T cells with tumor-suppressive function in the colon, such as effector CD8+ T cells and the ability of GPR15L administration to shrink established MC38 tumors in GPR15-sufficient but not in GPR15-deficient mice. The gene discussed is CD8A; the disease is neoplasm.