Ann: Further GvHD Clinical Data Published in Nature Medicine, page-7

Not really, as they couldn't get data from an MSC product that has been approved based on data in adults to compare it against: "the Janus kinase inhibitor ruxolitinib has been approved for the treatment of SR-aGvHD by multiple regulatory authorities, including the US Food and Drug Administration."
https://www.nature.com/articles/s41591-024-02990-z

They could have used the data from Japan, which reported "At 52 weeks, 12 patients (48 %) treated with MSCs only (six patients) and MSCs plus additional treatments (six patients) were alive in CR", but I couldn't see a follow-up for 18 months (I must admit I spend as much time looking for it as you did researching your post).
https://link.springer.com/article/10.1007/s12185-015-1915-9

Interesting is the reference to MSC-FFM, which is an approach taken in Germany that @JB1975 first mentioned years ago, and the results I have shared on here a few months ago, "Furthermore, a recent study of ‘real-world’ experience with a bone marrow-derived MSC product reported that the probability of overall survival in adults with ruxolitinib-refractory aGvHD after MSC treatment at 6, 12 and 24 months was 47% (38–56%), 35% (27–44%) and 30% (22–39%), respectively."
https://pubmed.ncbi.nlm.nih.gov/37990219/
Their approach is very interesting, since there starting material is not made from one donor (per Master Cell Bank), but instead "manufactured from pooled BM mononuclear cells from eight HLA-disparate healthy donors. MSCs are selected by plastic adherence, expanded in platelet lysate–enriched media in 2D culture to the end of passage 3, then frozen in saline-albumin with DMSO at a final concentration of 10% v/v until immediately prior to infusion."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664468/
This method may "average out" some of the hurdles brought up by the FDA and discussed by @JB1975 using graphs presented during the ODAC meeting:
"However, there is a high level of interdonor variability in the propensity of MSCs to be activated by IFNγ and TNF, and thus in their capacity to express indoleamine 2,3-dioxygenase5,6,7. MSC gene expression, differentiation, proliferation and colony-forming capacity are also donor-dependent and tissue source-dependent2,8."
https://www.nature.com/articles/s41591-024-02990-z
However, too early to say.

Shame that a positive article always ends up being used to try and cast doubt. Now and then, I am happy to "play ball", although being in a more moderate way now as usual.