As an example, an analysis of the pediatric AML molecular landscape found that mutations in the Muscleblind Like Splicing Regulator (MBNL1), Zinc Finger E-Box Binding Homeobox 2 (ZEB2), and E74-like factor 1 (ELF1) genes were disproportionately prevalent in pediatric AML tumors in comparison to adult AML tumors [9]. This evidence concerns the gene ELF1 and acute myeloid leukemia.