DOT1L and leukemia: This molecule showed high selectivity and the ability to reduce the level of H3K79 mono- and di-methylation in a dose-dependent manner, while also causing apoptosis increase in MLL-rearranged leukemia cell and deregulation of known DOT1L target genes such as HOXA9 and MEIS1, presenting a novel, highly potential, scaffold to exploit for DOT1L inhibitors development (Chen and Park, 2019).