In B-cell non-Hodgkin lymphoma (B-NHL), gene amplification of the PI3K (phosphatidylinositol-4,5-bisphosphate 3-kinase) subunit p110α, or loss  of its antagonist PTEN (phosphatase and tensin homolog) facilitate constitutive activation of PI3K and its downstream targets Akt/PKB and mammalian target of rapamycin (mTOR), which is associated with malignant transformation, tumor progression, and resistance against chemo- and radiotherapy1. Here, AKT1 is linked to neoplasm.