In CML, such as K562 cells, the constitutively active tyrosine kinase BCR-ABL promotes unregulated cell proliferation through phosphorylation signaling pathways that involve signal transducer and activator of transcription 5 (STAT5) and Crk-like proto-oncogene (CrkL). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.