Many believe that the 2003 SARS epidemic resulted from the emergence of a bat-like coronavirus that also recognized the ACE2 receptor from civets, Baric recalled. Then, through a second rare mutational step, the civetadapted virus acquired the ability to use human ACE2 for docking and entry. The resulting human-adapted strain was then thought to have circulated back and forth between civets and humans to mediate the expanding outbreak. The civet as an amplifying host in the open markets was clearly associated with the expanding epidemic. However, he continued, another, perhaps more likely, explanation for the initial emergence event was that bat SARS-like coronaviruses are naturally capable of recognizing ACE2 receptors from multiple species, including humans, civets, and a subset of other species (Graham et al., 2013). Once these generalists infect across species, additional mutations arose that permitted efficient crosstransmission between humans and civets as well as more efficient human-to-human transmission.