A central constituent of the innate immunity driving inflammatory responses in sepsis is the Toll-like receptor 4 [76], and we and others present different lines of evidence to ascribe a crucial role to TLR4 in the development of ALI in COVID-19 [16,17]; I) TLR4 constitutes a major sensor for pathogens as well as for endogenous alarmins including oxidized surfactant-derived phospholipids, and its activation in AMΦ was previously shown to promote hyperinflammation and ALI in mice [19]. This evidence concerns the gene TLR4 and acute respiratory distress syndrome.