This led to the hypothesis (hypothesis 1) that SARS-CoV-2-mediated downregulation of ACE2 disturbs the balance between ACE/AngII/AT1R and ACE2/Ang1–7/MasR signalling in the lungs and thereby contributes to the development of ARDS in COVID-19 patients (Fig. 2). The gene discussed is ACE; the disease is COVID-19.