The enhanced ADCC activity of bemarituzumab was also demonstrated by its >20-fold higher affinity for human FcγRIIIa compared to a fucosylated version of the antibody (FPA-144F), and its capacity (but not an ADCC-deficient version, bemaritzumab-N297Q) to suppress tumour growth and increase the recruitment of NK cells into the tumour microenvironment in a syngeneic mammary tumour model. The gene discussed is FCGR3A; the disease is neoplasm.