For example, in preclinical studies, pharmacologic inhibition of DOT1L has been reported to impair proliferation, to induce cell differentiation, or to impact gene expression of primary AML cells harboring IDH1/2 mutations (78) as well as AML cell lines and a xenograft model with partial tandem duplication (PTD) of MLL (MLL-PTD) (79). The gene discussed is DOT1L; the disease is acute myeloid leukemia.