The exact pathophysiological aspects underlying COVID-19-induced myocarditis are, so far, not clearly characterised, and several additional hypotheses have been suggested, including direct myocardial injury following the interaction between SARS-CoV-2 and ACE2, downregulation of ACE2 and consequent overstimulation of the renin–angiotensin–aldosterone system (RAAS) [14,21]. This evidence concerns the gene ACE2 and myocarditis.