FCGR3A and COVID-19: Evidently, SARS-CoV-2-specific IgG with a proinflammatory phenotype together with abundant circulating sICs could greatly enhance the pathogenic potential of FcγRIII/CD16 expressing T cells in COVID-19 disease and readily explain the uncontrolled and disseminated clinical presentation of the SARS-CoV-2 induced disease complex.