With no effective drug treatments for malignant glioma these tumours are invariably lethal. One key discovery in glioma biology is that the EGFR/RAS/PI3K axis is activated in most gliomas. Indeed, preclinical trials are underway for therapeutics targeting PI3K/AKT and RAS/RAF in malignant glioma. Unfortunately, these studies have already revealed rapid acquisition of tumour resistance, which highlights the importance of understanding the activity of downstream targets. Elevated FBP and MYC correlate with poor patient survival, which suggests FBP and MYC abundance/activity might also be drivers of glioma malignancy. This project builds on our exciting observation that FBP is a critical downstream target of EGFR/RAS/PI3K. We aim to use Drosophila, mouse and human glioma models to determine how the FBP-MYC axis drives MYC expression and brain tumour growth. Given the capacity of FBP knockdown to extinguish RAS-activated MYC expression, we propose that FBP is an attractive future target for developing novel cancer therapies.