Because COVID19-mediated stroke, and experimental stroke models are both thrombotic phenomena exhibiting deficits in ACE2/MasR signaling, the successful demonstration that SARS-CoV-2-induced ACE2 suppression mediates increased thrombotic risk and that stem cell ACE2/MasR activators may eliminate such risk could define highly novel, valuable, innovative, and safe approaches for clinically managing COVID-19 stroke, and other thrombotic complications of COVID-19 (pulmonary embolism). This evidence concerns the gene MAS1L and pulmonary embolism.