We genetically transduced the NK-92MI cells with human receptor CD16-BB-ζ (FcγRIIIa fusion protein) or human receptor CD64-BB-ζ (FcγRI fusion protein) to enable ADCC or ADCP activity in the presence of rituximab, or another therapeutic antibody in other tumor settings. The gene discussed is FCGR3A; the disease is neoplasm.