MECOM and myeloid neoplasm: During the attempt to correct mutations of gp91PHOX in hematopoietic progenitor cells, the vector integration resulted in EVI1 overexpression and the competitive outgrowth of mutated clones in 2 patients, eventually contributing to the development of myeloid malignancies.104 These cases formally illustrate the capacity of the EVI1 gene to initiate myeloid malignant transformation when aberrantly expressed in primary HSCs.