ABL1 and acute lymphoblastic leukemia: In B cell precursor ALL, we previously showed that combined suppression of PI3K, mTORC1 and mTORC2 displayed greater antileukemic activity than selective inhibitors of PI3K, mTORC1 or mTORC1 and mTORC2 irrespective of their genetic subtype and in case of BCR-ABL1 positive ALL their responsiveness to ABL-directed kinase inhibitors [46].