SLC44A4 and neoplasm: Specifically, it has been shown that CTL4 blockade depletes Treg populations while enhancing antitumor immunity through the expansion of tumor-infiltrating CD8 T and Th1-like CD4 effector cell populations.[15–17] Persistent antigen stimulation may eventually lead to CD8 cell exhaustion partly due to overexpression of inhibitory receptors such as PD-1, an effect that is abrogated by CPI allowing for reinvigoration of T-cell mechanisms.[5]