Using the early available data from COVID-19, that demonstrates comorbidities associated with high ACE2 levels are more likely to be infected, one can hypothesize that there are potential genetic variants that also influence the response to infection, given that common variants of renin, angiotensinogen, ACE and the Ang-II receptor have been shown to influence the function of the RAAS [14–18]. This evidence concerns the gene ACE and COVID-19.