Thus, they noticed that TLR3−/−, TLR3+/−, IRF7−/−, and IFNAR1−/− fibroblasts previously transduced with ACE2 and TMPRSS2 were more susceptible to SARS-CoV-2 infection in vitro vs. cells from control subjects but were rescued by transduction of wild type IRF7 or IFNAR1. All these data suggest that genetic defects in the pathway of type I IFNs may be key determinant of COVID-19 severity [113]. This evidence concerns the gene IFNAR1 and COVID-19.