The mechanism: a conventional dual inhibition of class I PI3K and mTOR kinases by capturing their ATP-binding sites. Effects: enhances the dexamethasone-induced apoptosis in ALL cells (preferentially T-ALL); down regulates Mcl-1 and increases BIM expression; enhances DEX efficiency in T-ALL xenograft models (the tumor load and burden decreases, the EFS increases). This evidence concerns the gene MCL1 and neoplasm.