FNDC3B (fibronectin type III domain containing 3B) is a multifunctional protein implicated primarily in cancer progression and metastasis. While UniProt suggests potential roles in adipogenesis, the published literature focuses predominantly on oncogenic functions across multiple cancer types. Mechanistically, FNDC3B operates through multiple pathways. In gastric cancer, FNDC3B interacts with FAM83H protein, preventing its proteasomal degradation and activating the EMT pathway to promote metastasis 1. In nasopharyngeal carcinoma, FNDC3B escapes microRNA-mediated repression through 3'-UTR shortening and stabilizes MYH9 protein to activate Wnt/β-catenin signaling 2. In hepatocellular carcinoma, E2F1 transcription factor regulates FNDC3B expression to promote cell migration 3. Notably, circular FNDC3B (circFNDC3B) acts as a tumor suppressor, competing with oncogenic FNDC3B mRNA through IGF2BP1 interaction 4. Clinically, elevated FNDC3B expression correlates with poor prognosis in gastric cancer, cervical cancer, and nasopharyngeal carcinoma, with high sensitivity for predicting disease progression 1 5. FNDC3B has been identified as a fusion gene partner in acute promyelocytic leukemia variants 6 and as a GWAS-identified locus associated with primary open-angle glaucoma 7. These findings establish FNDC3B as a potential therapeutic target across multiple malignancies.