Unlike traditional mAbs, which depend on the relatively transient interaction between their Fc region and CD16a, NKCEs establish more robust connections with a range of activating receptors (e.g., CD16a, NKG2D, NKp30, NKp46, NKG2C) and inhibitory receptors (e.g., Siglec-7) on NK cells, thereby increasing cancer cell killing efficacy and specificity. This evidence concerns the gene FCGR3A and cancer.