Given that genomic variation of HOXA9 including NUP98-HOXA9 fusion and gene amplification accounted for less than 2% of HOXA9 overexpression in AML cases (Xu et al., 2016; Gough et al., 2011; Nakamura et al., 1996), uncovering the upstream epigenetic and transcriptional regulators of HOXA9 in leukemia could advance the design of novel therapeutic interventions. Here, HOXA9 is linked to acute myeloid leukemia.