ACE2 and myocarditis: Although this could be an explanation of the post-vaccine pathophysiological dysfunctions, we suggest a simpler hypothesis also based on mimicry that could account for both rare myocarditis and thrombosis events reported post-vaccine against SARS-CoV-2 and postulate that interaction between the viral spike and ACE2 reduces ACE2 protease activity and increases Ang II, leading to lung cells hypoxia and dysfunction in the RAS pathway (thrombosis) (Figure 3).