In COVID-19 patients, SARS-CoV-2 binding to its ACE2 receptor and decrease in ACE2 availability creates an imbalance in the RAAS, resulting in the hyper-activation of AngII/AT1R axis and triggering the NF-κB activation mediated inflammatory process and synthesis and secretion of pro-inflammatory cytokines (TNFα, IL-6, IL-1, and IL-1β), which, in part, explains the severe disease manifestations, multi-organ failure, and higher mortality in diabetic COVID-19 patients [38,84]. The gene discussed is NFKB1; the disease is COVID-19.