Our major findings showed that HF blocked Akt1 activation by inhibiting its phosphorylation and kinase activity; suppressed Bad phosphorylation which can activate its pro-apoptotic function; activated the intrinsic pathway of cell death by targeting mitochondria, anti-apoptotic Bcl-2, pro-apoptotic Noxa, and caspases −9 and −3 in AML U937 cells. Here, BAD is linked to acute myeloid leukemia.