Intriguingly, we found that MTERF1 knockdown contributed to the decrease in ATP levels in CRC cells, thereby activating p-AMPK and then inhibiting p-mTOR and the downstream effector proteins of p-mTOR, p-P70S6K, and p-4E-BP1, indicating that MTERF1 regulates tumor cell proliferation by the AMPK/mTOR signaling axis. This evidence concerns the gene PRKAA1 and neoplasm.