Immunological component in the observed anti-tumor mechanism of mAb 1479 was probably minor, as xenografts were analyzed in the immunocompromised SCID background, mAb 1479 suppresses T-47D growth also in vitro[20], and since mAb 1479 is of the IgG2 isotype [20] that only weakly interacts with a single FcγR (FcγRII) leading to inefficient ADCC or complement activation [26]. The gene discussed is FCGR2A; the disease is neoplasm.