Whatever the outcome, it is tempting to speculate that the reduced proinflammatory activity of S1δ reported here would facilitate high viral loads (~1000 times higher) to be reached in the early stages of infection (46), together with its enhanced infectivity via cell surface entry facilitated by its increased efficiency to cleave the full-length S to S1 and S2 (47) and to fuse membranes at low levels of cellular receptor ACE2 (48). This evidence concerns the gene ACE2 and infection.