The vasculopathy observed in association with COVID-19 isn’t just an innate prothrombotic effect of the virus but also a consequence of the immune response of the host, through the release of pro-inflammatory mediators such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-a (TNF-a) that interact with the platelets and stimulate the expression of tissue factor (high-affinity receptor and cofactor for factor (F)VII/VIIa), eventually initiating the extrinsic coagulation cascade. The gene discussed is TNF; the disease is COVID-19.