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Leukemias driven by rearrangements of the lysine methyltransferase 2A (KMT2A, previously known as MLL) gene do not respond well to treatment and have a very poor prognosis (Krivtsov and Armstrong 2007; Milne 2017). KMT2A rearrangements (KMT2Ar) are chromosome translocations that fuse KMT2A in frame to one of a wide number of partner genes, creating novel fusion proteins (KMT2A-FPs), the most common of which is KMT2A-AFF1 (formerly MLL-AF4 or MLL-MLLT2) (Meyer et al. 2013). KMT2Ar leukemias have few cooperating mutations (Bardini et al. 2010, 2011; The Cancer Genome Atlas Research Network 2013; Andersson et al. 2015), thus the KMT2A-FP is able to drive leukemogenesis alone through aberrant gene expression profiles. KMT2A-AFF1 is most commonly associated with acute lymphoblastic leukemia (ALL) (Meyer et al. 2013) but can display a mixed phenotype with features of both acute myeloid leukemia (AML) and ALL (Alexander et al. 2018). A subset of ALLs, such as KMT2A-AFF1, can also relapse after treatment to become an AML derived from the original leukemic clone (Dorantes-Acosta and Pelayo 2012; Gardner et al. 2016; Pillai et al. 2019), which is indicative of a core KMT2A-AFF1 GRN that can drive both ALL and AML.

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