Indeed, microvascular healthy pericytes express ACE2,15,25,26 and this expression can be further increased in pathological conditions such as lung fibrosis,27 a clinical complication observed in patient cohorts known to be vulnerable to COVID-19 infection.28 The ability of SARS-CoV-2 to infect target cells is heavily dependent on the restricted expression of ACE2, TMPRSS2, and novel proteases and cofactors.19,26 Using vascular and kidney organoid models, Monteil et al.29 showed that SARS-CoV-2 can directly infect vascular organoids, which can be reversed by human recombinant soluble ACE-2. The gene discussed is ACE2; the disease is pulmonary fibrosis.