IGF2BP2 is an RNA-binding protein that functions as an m6A reader, recognizing the consensus GG(m6A)C sequence in thousands of mRNA transcripts 1. Unlike decay-promoting m6A readers, IGF2BP2 promotes mRNA stability and storage of target transcripts, including MYC, by binding through its K homology domains 1. This stabilization mechanism shields mRNAs from degradation and modulates their translation rates. IGF2BP2 demonstrates significant oncogenic potential across multiple cancer types. In acute myeloid leukemia, high IGF2BP2 expression associates with unfavorable prognosis and promotes leukemia stem cell self-renewal through m6A-dependent regulation of glutamine metabolism pathways 2. In cervical cancer, HPV E6/E7 proteins upregulate IGF2BP2 to enhance aerobic glycolysis via MYC mRNA stabilization, promoting tumor progression 3. Similarly, in colorectal cancer, METTL3-mediated m6A modifications depend on IGF2BP2 to stabilize glycolytic enzymes HK2 and GLUT1 4. In lung adenocarcinoma, tumor-derived exosomal IGF2BP2 activates endothelial FLT4 stability, promoting angiogenesis and metastasis 5. In pancreatic cancer, stromal stiffness stabilizes IGF2BP2, which upregulates sphingomyelin synthesis to enhance PD-L1 localization and immune evasion 6. Genome-wide association studies identified IGF2BP2 as a shared locus between type 2 diabetes and depression, suggesting broader metabolic roles 7.