The potential mechanisms for this phenomenon include infection of the hepatocytes expressing angiotensin-converting enzyme 2 (ACE2), “bystander hepatitis” as has been observed with other viral infections, and medications, but the damage is generally considered to be self-limiting.11,12 In our cohort, some patients had ALT elevation over more than two months from the onset of COVID-19. The gene discussed is ACE2; the disease is hepatitis A virus infection.