We also genotyped primary leukemias from Cux1+/−;Flt3ITD mice since copy-neutral loss of heterozygosity at the Flt3ITD locus leading to doubling of Flt3ITD gene dosage has been associated with disease progression in murine and human FLT3ITD-associated AML43,44, but we found no evidence of this phenomenon at either Flt3ITD or Cux1 loci (Fig. 3j), implying that heterozygosity for both alleles was sufficient to promote leukemogenesis. This evidence concerns the gene CUX1 and leukemia.