These data indicate for the first time that CD16-mediated stimulation by opsonizing auto-antibodies led to an amplified in vitro expansion of the FcεRIγ−CD16+ memory NK cell pool, due to a selective effect on both more (CD57+) and less (CD57−) differentiated NKG2C+ subsets, thus matching the in vivo altered composition of the FcεRIγ− pool in ITP patients (Figure 4A). This evidence concerns the gene FCGR3A and autoimmune thrombocytopenic purpura.