We had previously hypothesized that, by binding to ACE2, SARS-CoV-2 causes a dysfunction of this molecule, the consequence of which is the accumulation of Ang II and an activation of intracellular signals via AT1R, which are responsible for harmful events at the level of cell, tissues and organs to the point of being a major element of the physiopathology of COVID-19 [18]. This evidence concerns the gene AGTR1 and COVID-19.