Using a sensitive approach that is based on automated enumeration of DSB co-localizing proteins γH2AX and 53BP1, a higher γH2AX/53BP1 foci were detected in ALL patients harboring BCR-ABL or TEL-AML1 than patients without gene fusions, suggesting that BCR-ABL/TEL-AML1 induces DNA instability through facilitating further genetic alterations which drive leukemogenesis [49]. This evidence concerns the gene ABL1 and acute lymphoblastic leukemia.