For example, in chronic myeloid leukemia (CML), a reciprocal translocation (9;22)(q34;q11), known as “Philadelphia chromosome” (Ph), determines the formation of a fusion protein, B cell receptor (BCR)/ABL, that activates various intracellular pathways, such as signal transducer and activator of transcription 5 (STAT5) and phosphoinositide 3-kinase (PI3K) signaling pathways, leading to increased cell survival and proliferation. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.