CD8A and acute myeloid leukemia: Therefore, treatment with histone deacetylase inhibitor (HDACi) or silencing of <i>PAC1</i>, as a T cell-specific epigenetic modulator, significantly increased the expression of IC receptors and defined effector molecules in CD8<sup>+</sup> T cells.<h4>Conclusions</h4>Our results suggest that CD8<sup>+</sup> T cells in AML are dysfunctional mainly due to pathological epigenetic silencing of activating IC receptors rather than due to signaling by immune inhibitory IC receptors, which may explain the limited efficacy of antibodies that block immune-inhibitory ICs in AML.