When infected with SARS-CoV-2 in vitro, more infection occurred in cells from patients with mutant TLR3 alleles than in cells from healthy controls with wild-type TLR3. The addition of exogenous IFN-β largely removed this difference in SARS-CoV-2 infection efficiency, suggesting that IFN-β, which produced upon TLR3-mediated sensing of SARS-CoV-2, inhibits viral spread. The gene discussed is TLR3; the disease is infection.