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. Here, RUNX1 is linked to myeloid neoplasm.