AML cells upregulate inhibitory markers in order to escape from the immune system, such as PD-L1, which induces an exhausted phenotype on T cells characterized by the expression of lymphocyte-activation gene 3 (LAG3), programmed death receptor 1 (PD-1), cytotoxic T-lymphocyte associated protein 4 (CTLA-4) and TIM3 (Epperly et al., 2020; Zhu et al., 2022). This evidence concerns the gene CTLA4 and acute myeloid leukemia.