These data point to equivalent neutrophil-mediated phagocytic clearance of immune complexes across FcγR2B+3B− and FcγR2B−3B+ groups, probably due to equivalent FcγR2A binding, but striking differences in inflammatory responses after uptake, resulting in elevated cytokines and chemokines in the absence of FcγR3B, may contribute to inflammatory cascades, cellular infiltration and activation of immunity in the lung that may lead to COVID-19. The gene discussed is FCGR2A; the disease is COVID-19.