YTHDF1 is an N6-methyladenosine (m6A) reader protein that recognizes and binds m6A-modified mRNAs to regulate gene expression through multiple mechanisms. Functionally, YTHDF1 promotes translation of m6A-containing mRNAs by interacting with translation machinery 1, while also mediating mRNA degradation through interaction with AGO2 and promotion of phase-separated P-body formation 2. These dual functions enable dynamic control of protein production from m6A-marked transcripts 1. Mechanistically, YTHDF1 binds m6A-modified mRNA targets and promotes their translation efficiency 1, exemplified by EZH2 mRNA translation in hepatocellular carcinoma 3 and MeCP2 mRNA translation in cardiac fibrosis 4. Additionally, YTHDF1 recruits AGO2 through its YTH domain, facilitating P-body formation via liquid-liquid phase separation to promote mRNA degradation 2. Clinically, YTHDF1 overexpression correlates with poor prognosis in multiple cancers. In NASH-HCC, YTHDF1 drives tumorigenesis by promoting EZH2-mediated IL-6 secretion, recruiting immunosuppressive myeloid-derived suppressor cells and suppressing CD8+ T-cell function 3. YTHDF1 inhibition synergizes with anti-PD-1 immunotherapy 3. In neurodevelopmental disorders, YTHDF1 inhibition reverses fragile X syndrome defects caused by FMRP depletion 5. YTHDF1 dysregulation also contributes to pulmonary and cardiac fibrosis pathogenesis 64, suggesting therapeutic potential across multiple disease contexts.