In addition to RUNX1-mutated AML, BTX-A51 demonstrated activity in multiple other genetic mouse models of AML.(20) Although we did not observe responses among those without RUNX1 mutations, BTX-A51 treatment decreased MCL1 expression and increased levels of serum MIC-1, a biomarker of P53 activation. The gene discussed is MCL1; the disease is acute myeloid leukemia.