Taken together with our previous report that HF blocked NB4 proliferation and reduced the leukemia burden in vivo we postulated that despite the interference of PML/RARα with TFβR1/SARA/SMAD2/3 complex, the TGF-β pathway remain active in APL and contributes for leukemia progression. The gene discussed is TGFB1; the disease is acute promyelocytic leukemia.