Generally, all these studies found an association between a compromised antiviral response and uncontrolled inflammatory response mediated by hyperactivation of JAK-STAT, NF-κB, and TGF-β signaling pathways through overexpression of proinflammatory cytokines, including IL6, IL10, IL23A, TNF-α, and IL18, and COVID-19 severity [8–13]. The gene discussed is IL10; the disease is COVID-19.