The fusion protein product of the Bcr/Abl gene is a key factor in CML pathogenesis due to its sustained tyrosine kinase activity, which is able to stimulate numerous oncogenic signaling pathways, including the PI3K/AKT/mTOR, RAS/RAF/MEK/ERK, and JAK/STAT pathways [2]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.