ACE2 and viral infectious disease: Shapira et al. have now demonstrated that it is possible to therapeutically exploit a host cell process that is pivotal in SARS-CoV-2 infection.1 Viral infection not only requires binding of S to its receptor angiotensin-converting enzyme 2 (ACE2) but also cleavage of S at two distinct sites by host cell proteases: First, furin (and related pro-protein convertases) cleaves at a polybasic site, generating the S1 and S2 subunits, which remain non-covalently linked (S1/S2 site, Fig. 1a).