ADAM17 has been shown to shed ACE2 during SARS-CoV infection.26–28 However, in the setting of SARS-CoV-2 infection, we did not observe ACE2 in the cell culture supernatant, and ACE2 degradation was not inhibited when ADAM17 inhibitor TAPI-1 was added during pseudovirus infection (Supplementary Fig. S1e). The gene discussed is ADAM17; the disease is severe acute respiratory syndrome.