Notably, the FcεRIγ−NKG2C+CD57+ subset was significatively expanded in ITP patients, while the relative abundance of its FcεRIγ+ counterpart was comparable to that observed in healthy HCMV+ individuals (Figure 4A,B, respectively); the more immature FcεRIγ−NKG2C+CD57− subset was also increased in ITP patients, although to a lower degree. This evidence concerns the gene B3GAT1 and autoimmune thrombocytopenic purpura.