BCR-ABL genes were found in patients with certain types of leukemia and also detected in almost all patients with chronic myeloid leukemia (CML).63 Loss of auto-inhibition and constitutional activation of ABL1 may occur when the mutant BCR-ABL1 protein arises, with subsequent effects on signalling pathways related to cell cycle and apoptosis, such as the RAS/RAF/MEK/ERK pathway, the JAK2/STAT pathway, and the PI3K/AKT/mTOR pathway. This evidence concerns the gene SOAT1 and chronic myelogenous leukemia, BCR-ABL1 positive.