PD-1 signaling on specific T cells leads to T-cell exhaustion, and leukemia cells inhibit effector T-cell proliferation through PD-1/PD-L1 interactions, blocking PD-1 signaling contributes to improved CML control in pre-clinical mouse models by restoring the function of CML-specific CTLs (64). This evidence concerns the gene PDCD1 and chronic myelogenous leukemia, BCR-ABL1 positive.