Data obtained in preclinical tumor models suggest tumor-associated CD38 elicits resistance to the PD-1/PD-L1 blockade through the inhibition of CD8-positive T-cell activity, as was observed in an NSCLC in vivo model, thus explaining the observed significant efficacy of a PD-L1 inhibitor used in combination with CD38 antibodies [59,60]. Here, CD8A is linked to neoplasm.