In summary, we have found out and proved that samd3 from TGF-β pathway is a probable target for HHT, and through phosphorylating smad3 in the AML cell lines, HHT could active the TGF-β pathway, which in turn arrest the cell cycle at G1 phase or induce cell apoptosis depending on the background, and thus inhibit the proliferation of these cells. Here, SMAD3 is linked to acute myeloid leukemia.