COVID-19 progression is deemed as a consequence of complicated interplays among various pathophysiological mechanisms, such as direct cytopathic effects of SARS-CoV-2, dysregulation of the renin-angiotensin-aldosterone system (RAAS) and activation of des-Arg9-bradykinin (DABK) mediated by SARS-CoV-2-induced ACE2 inhibition, cytokine storm syndrome, autoimmunity and coagulopathy (Figure 2). The gene discussed is ACE2; the disease is COVID-19.