Attempting to decipher the molecular mechanism(s) by which the sequential combination of SAHA and DAC decreased cell viability and induced cell cycle arrest and apoptosis of AML cells, we first explored the protein expression levels of proapoptotic proteins involved in the intrinsic apoptotic pathway (caspase 9, Bax, and cytochrome c1) and the extrinsic pathway (caspase 8 and 3) and p21, a key regulator of cell cycle progression at G1 and S phases, in U937 cells, by western blot normalized to β-actin. The gene discussed is ACTB; the disease is acute myeloid leukemia.