Etiology: Chronic Myelogenous Leukemia (CML) originates from the Philadelphia chromosome, a genetic anomaly arising from a reciprocal translocation between chromosomes 9 and 22, denoted as t(9;22)(q34;q11). This translocation generates a chimeric gene, BCR-ABL, which encodes an aberrant tyrosine kinase. This hyperactive kinase drives the excessive proliferation of myeloid cells, leading to leukemia. Method for disease assessment: The clinical status of CML is assessed via Fluorescence In Situ Hybridization (FISH). FISH identifies the presence of the BCR-ABL fusion gene and the Philadelphia chromosome within patient cells, aiding in diagnosis and evaluating therapeutic efficacy.