Importantly, Kotini et al. modeled leukemic progression by engineering additional genetic lesions, either CRISPR-Cas9-mediated inactivation of the second GATA2 allele or chromosome 7q deletion, and showed phenotypic progression to low-risk and high-risk MDS, respectively (Kotini et al., 2017). This evidence concerns the gene GATA2 and myelodysplastic syndrome.