Although the etiopathogenesis of the symptomatology in patients with chronic COVID-19 is not clear, it has been hypothesized that these complications could be the consequence of direct tissue invasion by the SARS-CoV-2virus, possibly mediated by (i) the presence of angiotensin-converting enzyme receptor 2 (ACE-2), (ii) the exacerbated inflammatory response (also called cytokine storm), which is associated with damage to the immune system, or (iii) the state of hypercoagulability described in severe COVID-19. This evidence concerns the gene ACE2 and COVID-19.