This variance is critical in understanding the impact of COVID-19 at tissue/organ level with respect to susceptibility to COVID-19: higher ACE2 expression in the lungs of patients with diabetes might correspond to increased susceptibility to binding and subsequent replication of SARS-CoV-2, which in turn could drive a further up-regulation of ACE2, resulting in bradykinin and angiotensin 1–9-mediated pulmonary oedema [hypothesised here: (206)]. This evidence concerns the gene ACE2 and pulmonary edema.