Although not frequently mutated in prostate cancer Ras isoforms play a pivotal role in multiple pathways that have been implicated in prostate cancer progression to androgen independence. These have included growth factor and cytokine induced activation of the androgen receptor and its coregulators by post translational modification. Current evidence suggests that Ras is also required for androgen receptor activation in hormone sensitive cells. More recently Ras has been shown to work synergistically with other pathways to promote prostate tumorigenesis. We review the multiple lines of evidence implicating Ras as therapeutic target in androgen dependent and independent prostate cancer.