In order to extend our observations made in AML cell lines to primary models of STAG2-mutant myeloid disease, we developed a syngeneic mouse model in which Stag2 mutations arise as secondary lesions in the background of clonal hematopoiesis driven by tet methylcytosine dioxygenase 2 (Tet2) mutations, as is seen in the development of human MDS (4) (Figure 3A). This evidence concerns the gene STAG2 and myelodysplastic syndrome.