This regulatory process operates through two sequential mechanisms: (1) METTL1 deficiency decreases m7G-modified tRNA (e.g., LysCTT) abundance, inducing ribosome stalling at high-frequency codons (e.g., AAG) and preferentially suppressing translation of codon-enriched oncogenic transcripts like Cyclin-A2 (CCNA2) and Epidermal Growth Factor Receptor (EGFR); (2) Resultant translational repression reduces protein expression of cell cycle regulators (CCNA2, CDK6) and EGFR signaling components (EGFR, AKT, mTOR), ultimately inhibiting ICC proliferation and invasion (29). Here, CCNA2 is linked to intrahepatic cholangiocarcinoma.