Thus, it could be hypothesized that the upregulation in TLR downstream signaling molecules could be due to increased TLR/MyD88/NF-kB pathway in COVID-19 patients, of which TLR1 and 6 may participate through activation caused by beta-defensin-3, HMGB1 and S protein oligomannose-type glycans. The gene discussed is TLR1; the disease is COVID-19.