This translocation leads to a gene fusion between the Breakpoint Cluster Region (BCR) and the Non-Receptor Tyrosine Kinase ABL Proto-Oncogene 1 (ABL1), coding for a constitutively active tyrosine kinase, which essentially accounts for CML pathology [36]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.