Rare mutations, such as loss-of-function deletions in the genes coding for the participants of these pathways, causing deficiencies in the expression of TLR3, TICAM1 (Toll Like Receptor Adaptor Molecule 1), IRF3 and IRF7 (Interferon Regulatory Factors 3 and 7), and IFNAR1 and IFNAR2 (Interferon Alpha and Beta Receptor subunits 1 and 2), have been described as genetic factors underlying severe pneumonia in patients with COVID-19 [11, 12]. This evidence concerns the gene IFNAR1 and susceptibility to pneumonia measurement.