The malignant characteristic of CML, such as sustaining proliferation and apoptosis-resistance, attributes to the constitutively active BCR-ABL, which phosphorylates its substrates and activates several downstream signal pathways, including STAT5, MAPK and PI3K-Akt39. This evidence concerns the gene PIK3CG and chronic myelogenous leukemia, BCR-ABL1 positive.