Collectively, our data suggests that dual intron-targeting CRISPR-Cas9-mediated RUNX1-RUNX1T1 disruption represents a potential new future therapy modality for AML patients with t(8;21)(q22;q22.1), a gene therapy solution without a need for preceding fusion breakpoint sequencing as the only genetic information needed to qualify for treatment would be the standard diagnostic t(8;21) identification. This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.