To be clear that is not being disputed. IMO the central thesis of the paper is:
> the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans
That hypothesis is primarily supported by statistical evidence related to the frequency of certain amino acid mutations in the viral genome. For example:
> Considering that these two amino acid mutations are uncommon in human patients infected by non-Omicron SARS-CoV-2 variants (0.005% and 0.002%, respectively) we proposed the hypothesis that the progenitor of Omicron evolved in mice.
> searching against the GISAID database using Omicron’s backbone sequence. The top hits were again from the B.1.1 lineage, which differed from Omicron by 31 mutations, indicating that human SARS-CoV-2 variants reported to date could not provide a backbone for Omicron
While the paper certainly presents intriguing preliminary evidence, critically there was no analysis performed which accounted for variation or underestimates in viral mutation rates, number of infected hosts, or gaps in genomic DBs, etc. As such, there are certain hidden assumptions that were not explicitly addressed or conclusively proven.
Moreover, the "pleiotropic effect" is a significant confounding factor:
> predictions showed that the adaptation of Omicron to mice also promoted its adaptation to other species, such as humans, camels, and goats, via stronger RBD-ACE2 interaction (Fig. 6). Such a “pleiotropic effect” of mutations was likely caused by structural similarity of ACE2 across species
Finally, given that selective pressure due to mass distribution of S protein targeted vaccines was also not considered, I think it's fair to say that the evidence pointing to mice is fairly tenuous at this point. But the paper is still valid & interesting (I did not intend to suggest otherwise).