FCGR2A and infection: In this influential study, a variant of the bnAb b12 with Fc domain mutations designed to eliminate Fc receptor (FcγR) and complement initiator C1q binding (LALA) provided protection diminished from that of the unmodified antibody, while a C1q-only knockout (KA) variant demonstrated protection equivalent to that of unmodified b12, suggesting that FcγR- but not complement-mediated functions contributed to protection from infection in vivo (10).