Overall, the mechanisms by which the PI3K pathway is aberrantly activated, the relative contribution of different components of this pathway (PI3K, AKT, mTORC1 and mTORC2, S6 kinase etc.), positive and negative feedback mechanisms and the crosstalk with other signaling pathways differ substantially between tumor entities and between patients and cannot be assigned to specific subtypes. This evidence concerns the gene AKT1 and neoplasm.