Interestingly, ICAM1, which was the only persistent gene seen in both GWAS of sepsis and COVID-19 (Table S2), has known protein-protein interactions with the two hub genes NFKB1 and STAT3 and was also part of drug-gene sets of aspirin, thioridazine, pimozide, mefloquine, dexamethasone, and sulfasalazine (Table 2), suggesting these repurposed drugs may also modulate ICAM1. Several of the top persistently downregulated hub genes were ribosomal proteins (RPS6, RPS8, RPL5) indicating that ribosomal dysfunction might be another area to target therapeutically (Figure 5). This evidence concerns the gene NFKB1 and Sepsis.