The blockade of PD-1–PD-L1 interactions using clinical-grade human antibodies increases the proliferation and IFN-γ production of minor histocompatibility antigen (MiHA)-specific CD8 T cells when stimulated with PD-L1-expressing AML blast cells and DC, indicating that the PD-L1–PD-1 signaling pathway suppresses MiHA-specific CD8 T cell responses [19]. The gene discussed is PDCD1; the disease is acute myeloid leukemia.