The latter is known to have profound effects on therapeutic efficacy.48 A tumor with a high infiltrate of cells expressing activatory FcγR such as NK cells and macrophages, is likely to be more responsive to a mIgG2a mAb and depletion of detrimental target cells than a T-cell-agonizing mIgG1 mAb. The gene discussed is FCGR2A; the disease is neoplasm.