In a mouse model of AML, in which AML was induced by intravenous injection of C1498 (a murine leukemia cell line), elevation of PD-L1 on leukemia cells was observed, and less leukemia progression was achieved in PD-1−/− mice as well as by PD-L1 blockade.36 In the same mouse model of AML, coexpression of PD-1 and TIM-3 on exhausted CD8+ T cells was demonstrated and blockade of PD-1 and TIM-3 pathways synergistically improved relapse-free survival.30 Clinical studies using samples from AML patients are scarce. The gene discussed is CD8A; the disease is acute myeloid leukemia.