Some of the patient-derived mutations within either the N-terminal half of p85α (i.e. SH3 or BH domains) were able to alter Rab5 and/or PTEN regulation suggesting that they may contribute to oncogenesis and tumor progression, in addition to the more common p85α mutations within the C-terminal half that deregulate p110α-PI3K activity. Here, PTEN is linked to neoplasm.