The paired patient AML samples evaluated in this study harbored neither JAK2 nor FLT3-ITD mutations (Supplemental Table 1), and further investigation with additional samples or models will be needed to evaluate which JAK inhibitors are most potent in RUNX1mut disease and whether the presence of STAT5-activating mutations confers additional sensitivity or resistance in combination with RUNX1 mutations. The gene discussed is FLT3; the disease is acute myeloid leukemia.