Of note, IFNγ is an essential trigger of antimicrobial pulmonary responses, but increased IFNγ levels in COVID-19 blood and airways samples are associated with pathogenesis and pulmonary tissue damage (Chua et al., 2020; Karki et al., 2021; Montalvo Villalba et al., 2020), possibly through a detrimental effect of IFNγ on epithelial cells (Heuberger et al., 2021). This evidence concerns the gene IFNG and COVID-19.