As I understand it, that lineage of coronaviruses is quite distinct from the sarbecoronavirus lineage and they don't generally infect the same host species in the same geographical regions:
> "For coronaviruses, furin cleavage sites at the interface of the S1 and S2 domain are not unusual, being found widely in betacoronaviruses in the embeco lineage (which are considered to be of rodent origin) as well as in avian-origin gammacoronaviruses and certain feline and canine alphacoronaviruses (with an unknown origin). Furin cleavage sites are also found in certain bat-origin MERS-like merbecovirises, but not—with the exception of SARS-CoV-2—in the sarbecovirus lineage."
For such a specific motif to arise naturally seems to require a scenario like multiple infection of a host species by several different wild-type coronaviruses.
Then there's this feature:
> "So far, a viable natural origin for the SARS-CoV-2 S1–S2 site through recombination or mutation of a bat-origin virus has proved to be elusive. Of note, the S1–S2 cleavage site of SARS-CoV-2 S does not comprise the pattern found in prototypical furin cleavage sites (it is RRxR and not RxK/RR),8
making its origin enigmatic. One feature of the S1–S2 junction for the SARS-CoV-2 spike from the original outbreak is the presence of a leading proline residue, which might have promoted furin cleavage."
https://www.thelancet.com/journals/lanmic/article/PIIS2666-5...
At this point, the lab-accident-theory looks more likely than the natural-origin-theory.