In this regard, genomic studies of CUX1-mutated and -7/del(7q) myeloid malignancies have uncovered cooccurring inactivating mutations in other myeloid malignancy-associated genes such as TET2 and ASXL1 in addition to gain-of-function mutations in FLT3 and the RAS pathway, but their causal role in CUX1-deficient AML development is unclear19,25–27. The gene discussed is FLT3; the disease is myeloid neoplasm.