The coagulopathic profile of COVID-19 has been widely recognized and is largely attributed to a profound dysregulation of the coagulation cascade, primarily driven by an exaggerated inflammatory response known as the “cytokine storm”, with elevated levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1, IL-6, and other chemokines contributing to endothelial dysfunction, platelet activation, and hypercoagulability [5,6,7,8,9]. This evidence concerns the gene TNF and endothelial dysfunction.