Yet, whereas both Pten/Rb- and Akap12/Rb-null prostate lesions exhibit Akt activation (Fig. 2A) [3, 40], their mPC progression profiles differ (Table 1): Pten/Rb-null mice develop aggressive prostatic adenocarcinomas associated with systemic metastases, whereas Akap12/Rb-null mice develop HG-PIN plus local, indolent lymph node metastases. Here, AKAP12 is linked to prostate adenocarcinoma.