The rationale for targeting PD-L1 in AML stems from: (1) overexpression of PD-L1 in AML and MDS, the precursor of AML, and their association with poor prognosis (Figure S1) [36,37]; (2) PD-L1 enrichment in AML blasts at post-transplantation relapse; (3) PD-L1 orchestrated AML relapses after allogeneic hematopoietic cell transplantation (allo-HCT) [38] and (4) PD-L1 induced secondary resistance to hypomethylating agents (HMAs) in AML [39]. The gene discussed is CD274; the disease is acute myeloid leukemia.