Clarifying this point is all the more important for at least three reasons: (i) SARS-CoV2 was shown to acutely or chronically infect enterocytes in COVID-19 patients [24,25,26], (ii) ACE2 expressed by enterocytes exert mucosal immune functions that shape the composition of gut microbiota [27] and, potentially, the associated repertoire of microbiota-derived neuromediators [28], and (iii) patients with inflammatory bowel disease (IBD) exhibit both an intestinal down-regulation of ACE2 [29,30,31] and an abnormally high propensity to develop neuropsychiatric disorders [32,33]. This evidence concerns the gene ACE2 and COVID-19.