Figure 2

PI3K crosstalks with MEK and mTOR pathways. In addition to their divergent signalling cascades, these pathways converge on mTOR and drive a negative feedback loop on AKT regulation. For GBMs, combined PI3K/AKT and Raf-MEK-ERK inhibition might be required to shutdown mTORC1 signalling and promote apoptosis, autophagy and prevent cell growth. Tuberosclerosis 1 (TSC1 and 2); Tumour necrosis factor alpha (TNFα), hypoxia inducible factor (HIF1α), regulated in development and DNA damage response 1 (REDD1), 4E-binding protein (4EBP).