Regardless of how SARS-CoV-2 completes virion assembly, it is clear that membrane-bound ACE2 would play a physiological role in the replication of the novel virus. The question remains whether the use of ACE inhibitors, ARBs, and MRAs should be avoided in the setting of SARS-CoV infection because each agent (42, 43, 44, 45, 46,53) upregulates ACE2 expression and activity.