CTNNAL1 (catenin alpha like 1) is an adhesion molecule that functions as a scaffold protein modulating Rho pathway signaling, particularly through interactions with ARHGEF1 and YAP 1. Primary to its function is maintenance of airway epithelial structural integrity via the RhoA/ROCK1 pathway, regulating expression of adhesion molecules including E-cadherin, integrin β1, and integrin β4 2. CTNNAL1 promotes bronchial epithelial cell wound repair and proliferation through fibronectin-mediated focal adhesion kinase (FAK) phosphorylation 3. Mechanistically, CTNNAL1 inhibits epithelial-mesenchymal transition (EMT) by repressing Twist1 expression and reducing TGF-β1 secretion 4. It regulates mucus hypersecretion in asthma through YAP-ROCK2 signaling and controls CFTR expression via ROCK1-CAL pathways 56. Transcription of CTNNAL1 is induced during acute oxidative stress through AP-2α and LEF-1 recruitment to its promoter 7. Clinically, CTNNAL1 dysregulation associates with multiple diseases: genetic variants in CTNNAL1 confer susceptibility to Hirschsprung disease 1, while downregulation contributes to asthma pathogenesis through enhanced airway inflammation and mucus hypersecretion 56. CTNNAL1 was identified as a shared Rho-pathway biomarker linking postmenopausal osteoporosis and periodontitis 8.