Notably, in HER2-targeted breast cancer therapy, enhancing NK cell-mediated antibody-dependent cellular cytotoxicity (ADCC) via activating FcγRIIIa (CD16a) and macrophage-mediated antibody-dependent cellular phagocytosis (ADCP) through activating FcγRIIa (CD32a) and FcγRIIIa, alongside diminishing binding to inhibitory CD32b (FcγRIIb), has demonstrated enhanced cancer cell eradication [19,20]. This evidence concerns the gene FCGR3A and breast cancer.