While our results do not rule out a role for B55α loss in contributing to prostate tumorigenesis by activating AKT and/or inactivating pRB, the gain and loss of function studies with B55α-low PCa cells described here demonstrate that maintaining reduced levels of B55α is critically important for mitotic survival and open a novel potential avenue for therapeutic intervention. This evidence concerns the gene AKT1 and male reproductive organ cancer.