Among the causes of T-cell dysfunction in AML, a pivotal role is played by the frequent expression in blasts of co-inhibitory ligands, such as Gal-9, PD-L1, and CD155 [103], that, by binding their receptors on T-cells, lead to T-cell exhaustion, with the defective development of memory T-cells and T-cell deletion in the AML microenvironment [104], and, ultimately, disease progression [105]. The gene discussed is PVR; the disease is acute myeloid leukemia.