Here we reported that a loss of ABL1 could be also detected in a cohort of leukemias carrying AML1-ETO and NUP98-fusions and that murine hematopoietic cells expressing AML1-ETO and NUP98-PMX1 displayed accelerated proliferation and/or reduced differentiation in the absence of Abl1. This observation is supported by our previous report that normal ABL1 kinase exerted tumor suppressor activity in leukemias expressing oncogenic forms of the kinase such as BCR-ABL1, TEL-ABL1 and NUP214-ABL1 [11]. The gene discussed is BCR; the disease is leukemia.