Studies have highlighted that upon viral entry, SARS-CoV-2 engages with host ACE2 receptors and TMPRSS2 proteases, leading to viral entry and subsequent activation of NF-κB pathways and triggering of inflammatory cascades.475,476 The involvement of NF-κB in the outbreak stage of COVID-19 leads to an exaggerated inflammatory response characterized by the release of pro-inflammatory cytokines. This evidence concerns the gene NFKB1 and COVID-19.