NFKBIA’s downregulation in PBMCs of severe patients may be due to localization of cells expressing NFKBIA to the site of infection in attempts to regulate the hyperactive inflammatory state.(67) The upregulation of BCL2A1 and MTRNR2L12 is also indicative of extensive cellular stress.(68,69) While MTRNR2L12 is upregulated in both mild and severe disease, BCL2A1 is upregulated exclusively in severe disease. Here, NFKBIA is linked to infection.