FCGR3A mediates antibody-dependent cytotoxicity, and thus overexpression of this gene on the surface of immune cells mediates the release of cytotoxins and cytokines to kill target cells, and it is its immune activation that makes it potentially valuable for immunotherapy in AML (Li et al., 2022; De Taeye et al., 2020). This evidence concerns the gene FCGR3A and acute myeloid leukemia.