Furthermore, treatment with DNA methyltransferase inhibitors as well as DNMT1 knockdown enhanced ABCB1 expression while demethylating the promoter, thereby validating the functional significance of promoter hypomethylation in ABCB1 overexpression.<h4>Conclusions</h4>Our findings highlight ABCB1 promoter hypomethylation as a potential epigenetic driver of CFZ resistance in MM. This evidence concerns the gene DNMT1 and Miyoshi myopathy.