When lung tissues from SARS-CoV-2-high and -low samples were compared with those from nonviral ARDS, enrichment for S100A8 and S100A9 was observed, which is consistent with the significant enrichment of neutrophils in these samples and was previously suggested to be a driver of COVID-19 pathogenesis (Figure S4A).3 This evidence concerns the gene S100A8 and COVID-19.