EIF3F encodes a subunit of the eukaryotic translation initiation factor 3 complex that exhibits dual regulatory functions beyond canonical translation initiation. The protein demonstrates deubiquitinase activity, directly interacting with and stabilizing key metabolic enzymes through K48-linked deubiquitination 1. In hepatocellular carcinoma, eIF3f stabilizes ACSL4 to promote fatty acid biosynthesis and tumor progression 1. Similarly, in colorectal cancer, eIF3f enhances SGOC pathway reprogramming by deubiquitinating PHGDH and MYC, facilitating cancer development 2. The protein also forms complexes with YTHDF2 and DDX1 to enhance translation of m6A-modified mRNAs in ovarian cancer 3. In skeletal muscle, eIF3f serves as a central regulator of atrophy-hypertrophy balance, with overexpression promoting hypertrophy through mTORC1 pathway modulation 4. Loss of eIF3f function has tumor suppressive effects, inhibiting both cap-dependent and cap-independent translation while promoting rRNA degradation through interaction with hnRNP K 5. Clinically, homozygous missense variants in EIF3F cause autosomal recessive intellectual developmental disorder characterized by developmental delays, behavioral problems, hearing loss, and variable dysmorphic features 6.