markers such as Nrp1 and helios. Previously, MSCs were found to be associated with increased prevalence of induced Tregs (iTregs), as manifested by the low expression of the above two markers.2 Would the authors agree that this finding would be important toward identifying the mechanism of the beneficial effect of MSCs in ischemic kidney injury? Moreover, the immunosuppressive mechanism of Tregs can be contact-dependent or -independent (e.g., IL-10or TGFb-mediated). Would the authors agree that conducting transwell experiments with MSCs and splenocytes might help explain such a mechanism? Was there evidence of increased production of IL-10 or TGFb in the supernatants of coculture experiments? The authors presented data showing that a significant reduction in the percentage of IFNg-producing CD8 (more than CD4) was found in animals treated with MSCs. Subsequent coculture experiments confirmed that such an effect was attributed to the induction of Treg frequency. Previously, MSCs were shown to induce regulatory CD8Foxp3þ T cells.3 However, the authors did not report on the frequency of CD8Foxp3þ T cells as a potential explanation for the marked reduction in IFNgþCD8 T cells.