Exploration of the functional relationship between STAT3 and mTORC1 signaling in the metastatic PCa mouse model revealed a significant increase in protein levels of mTORC1 downstream substrates p-4E-BP1, 4E-BP1 and the phosphorylated ribosomal protein S6 in Ptenpc−/− Stat3pc−/− mice compared to Ptenpc−/− Stat3C/+ mice (Fig. 2D, E), supporting the role for STAT3 as a negative regulator of mTOR signaling in PCa. The gene discussed is RPS6; the disease is posterior cortical atrophy.