Targeting MUC1-C with silencing or pharmacologically with the inhibitor GO-203 in AML cell lines and primary blasts was thus associated with (i) the suppression of DNMT1, (ii) decreases in methylation of CpG islands in the CDH1 promoter, and (iii) upregulation of E-cadherin [2]. Here, DNMT1 is linked to acute myeloid leukemia.