This BCR-ABL SH2 domain deletion mutant renders myeloid cells lines IL-3 independent [17], [18], [19], and induces a lymphoid leukemia or a CML-like disease in mice, but the disease latency is increased as compared to full length BCR-ABL [20]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.