A recently reported person with deletion of FCRG3A in one chromosome and fusion of FCGR3A with FCGR3B in the other lacked CD16A on NK cells and NK cell-mediated ADCC, had persistent Epstein Barr virus (EBV) infection and renal failure, and had abnormally high percentages of NK cells with an early-differentiated phenotype (CD56dimNKG2A+NKG2D+CD94+CD57−KIR−) associated with acute EBV infection [17], and low percentages of memory-like or adaptive (CD56dimCD57+NKG2C+ and CD56dimCD57+FcRγlow/−) NK cells [18]. This evidence concerns the gene FCGR3A and acute kidney injury.