AML blasts have developed immunoediting processes, such as genetic deletion of HLAs, especially in the context of the haploidentical transplant, and epigenetic downregulation of HLA class II molecules in different donor transplant settings, which preclude conventional recognition of AML blasts by CD8 and CD4 T cells via αβTCR engagement with peptides presented in class I and II. The gene discussed is CD8A; the disease is acute myeloid leukemia.