In addition, some evidence suggests that endothelial cell activation might be also directly induced by SARS-CoV2 particles, due to the high levels of ACE2 and TMPRSS2 expressed by the endothelium [53] Finally, through its binding to ACE2, COVID-19 seems to induce both the overstimulation and imbalance of the Renin-Angiotensin-Aldosterone System, which can further contribute to vessel contraction and pro-hypertrophic and pro-fibrotic responses of endothelial cells [54]. This evidence concerns the gene TMPRSS2 and COVID-19.