An uncontrolled production of proinflammatory mediators, such as IL-6, IL-1β, IFN-γ, and TNF-α [25], drives hyperinflammation during severe COVID-19 infection, leading to cardiovascular and respiratory complications, including ARDS, disseminated intravascular coagulation [26], and heart failure [27]. This evidence concerns the gene TNF and acute respiratory distress syndrome.