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]. The gene discussed is ZEB2; the disease is acute myeloid leukemia.