The first is a homozygous point mutation (L66H) in FCGR3A, associated with decreased NK cell-mediated spontaneous cytotoxicity but intact ADCC [5], binding of CD16 by mAb 3G8 but not mAb B73.1 [5, 23], and clinical manifestations of frequent upper respiratory infections, recurrent HSV stomatitis, recurrent herpes whitlow, and EBV-associated Castleman’s disease [5]. Here, FCGR3B is linked to respiratory tract infectious disorder.