IFNAR1 and COVID-19: Studies have shown that greater levels of NLRP3 inflammasome activation in peripheral blood corresponded with more severe COVID-19 [37], that low expression of the IFNAR2 gene (an IFN 1 receptor subunit) was associated with critical illness in COVID-19 patients [38], that loss-of-function mutations in an another IFN I receptor subunit (IFNAR1) was associated with severe COVID-19 cases [39], and that auto-antibodies to IFN I were identified as a potential factor for severe COVID-19 [40].