Several hypotheses have emerged to explain the pathogenesis of COVID-19-related neurological disorders, with CMBs posited as a consequential late-stage manifestation of severe hypoxaemia in affected patients.21-23 Although the precise pathophysiological mechanisms remain elusive, one prevailing theory suggests that SARS-CoV-2-inflicted endothelial damage—mediated by the virus’s interaction with angiotensin-converting enzyme 2 (ACE2)—leads to a cascade of events. This evidence concerns the gene ACE2 and COVID-19.