Liu et al. found AD-MSCs from a T2DM ApoE−/− mouse model which performed a hypofunction in suppressing CD4+T lymphocyte proliferation and pro-inflammatory polarization partly due to immune phenotypic changes, cause by AD-MSC immune phenotypic changes with higher MHC-II, CD40, and CD80 [94]. This evidence concerns the gene APOE and Alzheimer disease.