Kornblau et al. identified that AML patient-derived BM-MSCs are more senescent than normal BM-MSCs [127], which might be due to the overexpression of Gal-3 protein by TGF-β induction in AML patient-derived MSCs, as senescent MSCs express and secrete high levels of TGF-β [143] and Gal-3 [144]. Here, TGFB1 is linked to acute myeloid leukemia.