Another TKI activating the PI3K/Akt/mTOR pathway is PDGFR. Imatinib blocks the ATP-binding site of tyrosine kinase proteins including PDGFR and inhibits the activity of PDGFR. The clinical efficiency of imatinib against other cancers such as chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GISTs) has been demonstrated [52–54]. Here, PDGFRB is linked to chronic myelogenous leukemia, BCR-ABL1 positive.