The binding of the virus to ACE2 leads to its internalization, causing an imbalance between ACE/ACE2, resulting in an unopposed higher level of Ang II and changing Ang 1–7/Ang II, which overactivates the AT1R and by losing the protective effects of the Ang 1–7/Mas R, it starts an inflammatory process that leads to a so-called cytokine storm and initiation and progression of ALI and ARDS [10]. Here, ACE2 is linked to acute respiratory distress syndrome.