Interestingly, treatment with the HDAC1 inhibitor AR-42 in Kasumi-1 and NB4 cells and leukemic blasts obtained from primary AML patients resulted in the downregulation of miR-29b targets, including Sp1, DNMT1, DNMT3A, and DNMT3B. This evidence concerns the gene DNMT1 and acute myeloid leukemia.