The pathogenesis of BCS primarily involves a hypercoagulable state, which may be inherited (e.g., Factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiencies) or acquired (e.g., APS, myeloproliferative disorders, pregnancy, infections such as COVID-19) [[11], [12], [13], [14], [15]]. This evidence concerns the gene F2 and COVID-19.