Cingulin (CGN) is a cytoskeleton-associated protein that plays critical roles in tight junction regulation and cellular structure maintenance. CGN is localized at apical cell junctions of epithelial cells, where it interacts with major cytoskeletal filaments and regulates RhoA activity 1. In auditory function, CGN is essential for maintaining cochlear hair cell structures, with enriched localization at hair cell cuticular plates and circumferential belts. Mutations in CGN cause autosomal dominant non-syndromic hearing loss through impaired hair cell cuticular plate morphology and hair bundle structure 1. Beyond its structural roles, CGN functions as an RNA-binding protein that promotes oncogenic processes in pancreatic ductal adenocarcinoma (PDAC). CGN stabilizes mRNAs of AXL and importin-7, activating MAPK/ERK signaling and facilitating nuclear translocation of phosphorylated ERK, which drives pancreatic cancer cell proliferation, gemcitabine resistance, tumorigenesis, and metastasis 2. CGN also promotes pancreatic acinar-to-ductal metaplasia and is progressively upregulated during PDAC progression, with overexpression correlating with poor patient prognosis 2. These findings establish CGN as both a critical structural protein for epithelial barrier function and hearing, and a significant oncogenic driver in pancreatic cancer.