Massie and colleagues showed that the AR regulated MPC activity via direct transcriptional control of MPC2. In AR-driven prostate adenocarcinoma, MPC inhibition led to reduced OXPHOS, activation of the eukaryotic initiation factor 2 α (eIF2α)/activating transcription factor 4 (ATF4) integrated stress response, and increased glutaminolysis [33]. Here, ATF4 is linked to prostate adenocarcinoma.