Obtained results clearly demonstrate that: first, there is a certain translational bridge between regulomes of ALI in mice and human; second, the group of influenza A-induced ALI in patients is the most enriched with mice-specific ALI-related key genes compared to groups of bacterial pneumonia and ARDS (Fig 3F); and, third, innate immunity regulators RSAD2, IFI44 and RTP4, showing key nodal positions within both influenza A- (Fig 3F) and SARS-CoV-2-related (Fig 3B) gene networks, can be considered as novel key regulators of virus-induced ALI/ARDS in human. This evidence concerns the gene RTP4 and bacterial pneumonia.