The absence of biochemically deleterious TLR8 variants in our cohort of patients with critical COVID-19 (Fig. S2) and its lack of expression on pDCs suggest that TLR8 is not a modifier of the SARS-CoV-2-related clinical phenotype of TLR7 deficiency, although it is adjacent to TLR7 on the X chromosome and can be stimulated by overlapping molecules. The gene discussed is TLR8; the disease is COVID-19.