AML’s distinct properties, including myeloid cell origin and immunosuppressive effects67 via production of reactive oxygen species and other soluble factors, may distinctly redirect T cells toward functional impairment that precludes transitioning to a classical exhausted phenotype and explain the observed NKL skewing in TTCR-C4 and endogenous CD8+ T cells. This evidence concerns the gene GLIS2 and acute myeloid leukemia.