Studies with Ts1Rhr mice which contain a triplication of a segment of mouse chromosome 16 that is orthologous to human chromosome 21 and serve as models for Down syndrome, and analysis of cells derived from a transgenic mice overexpressing human HMGN1 [51] provide evidence that HMGN1 overexpression promotes B-ALL. Here, HMGN1 is linked to precursor B-cell acute lymphoblastic leukemia.