Since severe COVID-19 is characterized by significant distortion of the lung angioarchitecture, small vessel vasculitis and microthrombosis, all associated with worse prognosis and increased mortality [40], we can theorize that SEMA3C might play a role in aberrant angiogenesis associated with the development of severe ARDS that is still to be investigated. The gene discussed is SEMA3C; the disease is acute respiratory distress syndrome.