The data did not support TGF-β auto-induction as the major mechanism of the benefits provided by BM-MSCTGF-β, suggesting different doses of TGF-β (3 ng/mL vs. 50 ng/mL) and cell origin (human AD-MSC vs. mice BM-MSC) had impacts on the downstream effects that TGF-β may inflict on MSCs. The gene discussed is TGFB1; the disease is Alzheimer disease.