Our most potent and selective dual BCL‐2/HDAC1 inhibitor BD‐4‐213 and BCL‐2/HDAC6 inhibitor AMC‐4‐154 inhibited the metabolism/viability of three AML cell lines more potently than did the parent BCL‐2 inhibitor venetoclax. Here, HDAC1 is linked to acute myeloid leukemia.