Apart from PTEN mutations, FLT3 mutations induce proliferation in AML through mTOR signaling, whereas in CML, BCR-ABL kinase binds to the p85 PI3K regulatory subunit, thereby activating the PI3K/Akt/mTOR pathway [24]. This evidence concerns the gene PIK3CA and chronic myelogenous leukemia, BCR-ABL1 positive.