Prostate cancer is the second most common cancer in the UK, and the second most lethal cancer in men. Treatment of prostate cancer is challenging because clinically similar tumours give rise to diverse clinical outcomes, and there are no reliable markers to discriminate tumours that will grow slowly from those which are aggressive and likely to spread. However, the tumour suppressor PTEN is lost in 40-80% of prostate tumours, and these tumours are usually more severe. Biochemically, PTEN dephosphorylates the 3 position of the inositol ring of phosphatidylinositol 3,4,5-trisphosphate (PIP3) to produce phosphatidylinositol 4,5-trisphosphate (PIP2). This opposes signalling through the AKT/MTOR pathway, which is a key regulator of cell growth, division and survival. However, the identity and significance of other pathways that are controlled by PTEN are unknown. Our lab has developed a mutant of PTEN (Y138L), which is able to control AKT signalling, but which is unable to regulate other signalling pathways which are normally controlled by PTEN. In the current work, we have used this mutant as a tool to investigate the relative importance of AKT independent signalling in the development of prostate cancer, using a mouse model.