PE engages multifactorial unified pathogenesis, which includes increased risk of thrombosis secondary to increased cytokines, endothelial injury, platelet activation, neutrophil traps, complement activity, hypoxia, and invasion of COVID-19 into the endothelial cells via angiotensin-converting enzyme 2 (ACE2) receptors as well as the presence of antiphospholipid antibodies[8]. This evidence concerns the gene ACE2 and COVID-19.