In a murine model studying ASXL2 loss in the context of the AML1/ETO oncofusion, ASXL2 functions as a haploinsufficient tumor suppressor when mice are challenged with either the full-length (AE) or short (AE9a) splice isoform of AML1/ETO [94]. The gene discussed is RUNX1T1; the disease is neoplasm.