This opinion was initially based on experimental results showing that in nude mice knocked-out for Fcγ receptor, the anti-HER2 and anti-CD20 mAbs were inefficient to treat human tumours expressing the relevant target antigens [29], and second, on the clinical observations of a correlation between FcγR3A genetic polymorphisms and response to mAb therapy [30,31]. This evidence concerns the gene FCGR3A and neoplasm.