ACE2 is highly expressed in different tissues, including lung pneumocytes, enterocytes, endothelial cells, and cardiomyocytes [29], and the interaction between SARS-CoV-2 and ACE2 results in the downregulation of the protective ACE2 with the initiation of hyper-inflammation and oxidative stress, that cause acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and multiorgan failure [30–32]. Here, ACE2 is linked to acute respiratory distress syndrome.