In CML, there is 5–15% association with Philadelphia chromosome, which results from a reciprocal translocation between chromosome 9 and 22 resulting in the formation of a BCR-ABL fusion protein thay encodes for the tyrosine kinase pathway, and this causes uncontrolled cell division, inhibition of DNA repairs, genomic instability, and the commencement of CML with induction of blast crisis. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.