In this study we demonstrated that HDAC1/2-selective inhibitors, namely ACY-957 and ACY-1035 of the biaryl aminobenzamide class, inhibited the viability of AML cells, increased their expression of the differentiation marker CD11b, and induced cell cycle arrest and apoptosis, both as single agents and in combination with azacitidine. Here, HDAC1 is linked to acute myeloid leukemia.