In addition to mediating PI3K-dependent signaling, AKT, PTEN and mTORC1/2 have also been shown to play a role in PI3K-independent signaling events (reviewed in [23,33,34,35,36]), and the PI3K-AKT-mTOR cascade interacts with multiple cooperative signal transduction cascades via a series of partially understood interactions and feedback loops to promote tumor growth (including MAPK, AR and WNT signaling, Figure 1). The gene discussed is PIK3CB; the disease is neoplasm.