From the pathophysiology perspective of COVID-19, SARS-CoV-2 induces direct cell toxicity, dysregulation of RAAS and kallikrein-kinin system, endothelial cell damage associated with thromboinflammation and thromboembolic events, dysregulation of the immune system characterized by hyperactivation of the innate immune system, hyper inflammation caused by inhibition of interferon signaling, T cell lymphodepletion by exhaustion, and the production of proinflammatory cytokines, particularly IL-6 and TNFα, which ultimately lead to cytokine storm [30,31]. The gene discussed is TNF; the disease is COVID-19.