For example, HDAC and histone methyltransferase inhibitors (e.g., against DOT1L), both of which associate with the MLL complex, have entered clinical trials for acute myeloid leukemia (Daigle et al., 2011; Chen et al., 2013; Fredly et al., 2013; Morabito et al., 2016), whereas negative regulation of oncogenic c-MYC has been achieved, for example, by inhibitors of BRD4 (such as JQ1) which displace BRD4 from the c-MYC promoter (Fowler et al., 2014). This evidence concerns the gene MYC and acute myeloid leukemia.