In AML, bone-marrow-infiltrating T-cell populations are preserved and may even be increased compared with bone marrows from healthy individuals, with an increased frequency of immune inhibitory and activating co-receptor expression (especially in relapsed AML), including PD-1, OX40, TIM3, and LAG3, suggesting a potential role for T-cell-harnessing therapies in AML [60–62]. The gene discussed is TNFRSF4; the disease is acute myeloid leukemia.