Although these mice do not develop MDS or AML, they express defective splicing of genes recurrently mutated in MDS/AML, such as GNAS, PICALM, H2AFY, BCOR, KDM6A, KMT2D (MLL2), and MED24, thus likely contributing to the altered hematopoiesis that is characteristic of MDS patients [31]. The gene discussed is KMT2D; the disease is myelodysplastic syndrome.