Nonetheless, AF anti-CD20 activated neutrophils more efficiently than fucosylated anti-CD20 in the presence or absence of FcγRIIIB (which is a glycosylphosphatidylinositol (GPI)-anchored decoy receptor), indicating AF hIgG1 can activate neutrophils via FcγRIIIA [36], as other FcγRs (FcγRI and FcγRIIA/B) do not differentiate AF vs. fucosylated antibodies [20, 37]. The gene discussed is FCGR3A; the disease is atrial fibrillation.