As Hoepel et al. show prolonged presence of afucosylated IgG in some individuals38 and as systemic inflammation in SLE has been linked to an increase in afucosylated IgG79, it is tempting to speculate that the formation of sICs in predisposed patients initiates a vicious cycle of FcγR-mediated inflammation leading to enhanced afucosylated IgG and FcγR activation by SARS-CoV-2-specific IgG, further contributing to inflammation and, conceivably, to de-novo sIC formation. The gene discussed is FCGR2A; the disease is systemic lupus erythematosus.