The increased FCGR3B copy-number, concomitant to CNR1 duplication, possibly confers augmented neutrophil adhesion and immune complex uptake; similarly, common finding of the higher-activity CD16B-HNA-1a variant could derive from selective pressures favouring immune complex clearance by high phagocytosis variants, most probably related to infectious disease burden, as previously suggested (2, 55). This evidence concerns the gene FCGR3B and infectious disease.