Emerging data have also indicated that tumors develop resistance to PD1/PD-L1 blockade by upregulating CD38 that inhibits effector T cell function through adenosine receptor signaling and inhibiting CD38 overcomes resistance in tumor models.[93] Based on promising results in the preclinical studies, CD38 antibodies have now entered early-phase clinical trials. This evidence concerns the gene CD38 and neoplasm.