Emerging research suggests that the overwhelming immune activation during SARS-CoV-2 infection is a potent catalyst for significant arterial and venous thromboembolism leading to strokes and pulmonary emboli [15, 38], and serum pro-inflammatory cytokines including IL-1β, TNF-α, and IL-6 have been tied to endothelial damage underlying thrombus formation seen in COVID-19 [39]. Here, TNF is linked to venous thromboembolism.