Patients with severe COVID-19 have a higher proportion of afucosylated anti-RBD antibodies, which bind FcγRs more avidly, and viral immune complexes containing these antibodies triggered more potent innate immune cell activation and release of proinflammatory cytokines, such as interleukin-6 (IL-6), IL-1β, and tumor necrosis factor (57, 58). This evidence concerns the gene IL1B and COVID-19.