However, the findings that overexpression of truncating mutation in hematopoietic cells of mice displayed human MDS features with de-repression of Hoxa9 in another study [19] and detectability of truncating proteins in human cell lines bearing ASXL1 truncating mutations argued for gain-of-function or dominant negative effects of ASXL1 mutations [19, 20]. This evidence concerns the gene ASXL1 and myelodysplastic syndrome.