In light of the many reports showing autoantibody formation in COVID-19 and the recent discovery of sICs being present in patient circulation [43], it is highly likely that severe COVID-19 follows a similar, if not even higher, combined local IC and systemic sIC driven immunopathology as observed in SLE where both ligands lead to excessive FcγRIIIA/CD16 activation. The gene discussed is FCGR3A; the disease is systemic lupus erythematosus.