PCa cells and stromal components sustain a hypermetabolic state characterized by heightened dependence on glutamine and mTORC1-mediated suppression of autophagy, a process critical for oncogenesis, as evidenced by dysregulated autophagy-related genes (e.g., STK11/LKB1) upstream of mTORC signaling (198). Here, STK11 is linked to posterior cortical atrophy.