NK cells doubly contribute to the therapeutic efficacy of tumor-targeting mAbs; besides the killing of tumor cells mediated by the engagement of the low affinity receptor for IgG, FcγRIIIA/CD16, activated NK cells secrete pro-inflammatory cytokines and chemokines which act in boosting the recruitment and activation of other immune effector cells and the development of long-lasting T cell immunity [2, 3]. The gene discussed is FCGR3A; the disease is neoplasm.