IGF2BP3 is an m6A-reader RNA-binding protein that stabilizes target mRNAs by recruiting them into cytoplasmic ribonucleoprotein complexes, protecting transcripts from degradation and modulating their translation 1. IGF2BP3 preferentially recognizes N6-methyladenosine-modified mRNAs and increases their stability 1, while also binding internal m7G modifications to promote transcript degradation in specific contexts 2. Clinically, IGF2BP3 drives multiple cancer-associated phenotypes through metabolic and epigenetic reprogramming. In hepatocellular carcinoma, lactylation of IGF2BP3 enhances its binding to PCK2 and NRF2 mRNAs, promoting lenvatinib resistance via antioxidant pathway activation 3. In non-small cell lung cancer, IGF2BP3 stabilizes COX6B2 mRNA in an m6A-dependent manner, increasing oxidative phosphorylation and conferring EGFR-TKI resistance 4. IGF2BP3 also promotes immune escape in breast cancer by stabilizing PD-L1 mRNA through METTL3-mediated m6A modification 5. Additionally, IGF2BP3 enhances lipid metabolism in cervical cancer by upregulating stearoyl-CoA desaturase through m6A-dependent mechanisms 6, promotes AML progression via IGF2BP3-SENP1-HDAC2-AKT signaling 7, and drives lung cancer metastasis by stabilizing MCM5 mRNA to activate Notch signaling 8. These findings establish IGF2BP3 as a critical oncogenic regulator linking epitranscriptomic modifications to metabolic reprogramming and therapeutic resistance.