Abstract: T cell dysfunction is a common feature in patients with acute myeloid leukemia (AML). The up-regulation of immune checkpoint (IC) proteins resulting in T cell exhaustion is a key reason for T cell dysfunction. Immunotherapy with IC inhibitors exerts a remarkable effect on AML. However, due to the heterogeneity of T cell exhaustion and other factors that impair T cell function in patients with AML, the optimization of targeted T cell immunotherapy strategy for AML might be based on the multidimensional investigation of immune deficiency with different T cell subtypes.