YTHDF3 is a cytoplasmic m6A reader protein that functions as an m6A-binding protein critical for post-transcriptional gene regulation. Mechanistically, YTHDF3 recognizes N6-methyladenosine (m6A) residues on target mRNAs and promotes their translation in synergy with YTHDF1 1, while cooperating with YTHDF2 to regulate m6A-modified mRNA decay 1. YTHDF3 undergoes liquid-liquid phase separation when binding polymethylated mRNAs, sequestering them into P-bodies and stress granules where compartment-specific regulation occurs 2. Beyond canonical mRNA translation, YTHDF3 drives cap-independent translation of circular RNAs through m6A recognition in an eIF4G2-dependent manner 3. In disease contexts, YTHDF3 overexpression promotes breast cancer brain metastasis by enhancing translation of m6A-enriched transcripts encoding ST6GALNAC5, GJA1, and EGFR 4. Post-translational palmitoylation of YTHDF3 by ZDHHC20 stabilizes MYC mRNA, driving pancreatic cancer progression 5. Conversely, decreased YTHDF3 expression in aged oocytes impairs meiotic maturation and maternal factor translation 6, while METTL3-dependent m6A methylation requires YTHDF3 for PTX3 mRNA degradation in macrophage homeostasis during allergic asthma 7. YTHDF3 thus functions as a context-dependent regulator of m6A-modified transcript fate with broad implications for cancer progression, reproductive aging, and inflammatory disease.