The rationale was threefold: first, although ALDH1A3 expression is a marker of reduced Foxo activity, Foxo is not absent in the majority of these cells, and complete Foxo ablation may exacerbate their phenotype; second, it may reduce heterogeneity of ALDH+ cells; and third, because Foxo-deficient mice develop a MODY-like form of diabetes, this comparison might reveal qualitative differences between ALDH+ cells isolated from euglycemic versus diabetic animals. Here, ALDH1A3 is linked to diabetes mellitus.