BM stromal cells induce ALDH activity in AML cells through increased expression of the ALDH2 isoform. BM-MSCs secrete TGF-β1, which exerts its effect through a noncanonical/p38-dependent signalling mechanism, leading to a stem-like phenotype in AML cells. Inhibition of downstream targets of this pathway, such as p38 MAPK, inhibits ALDH activity in AML cells. ALDH2 inhibition sensitizes AML cells to standard cytarabine chemotherapy in vitro. However, these findings were not validated in vivo. This evidence concerns the gene TGFB1 and acute myeloid leukemia.