These findings have 2 implications: 1) targeting αVβ8 integrin could suffice to prevent TGF-β activation in PCO; 2) the resulting attenuation of fibronectin fibril deposition (likely mediated by α5β1 integrin) may contribute to the long-term prevention of fibrotic PCO, as we have previously reported that fibronectin assembly is required for sustained LC fibrosis PCS (23). The gene discussed is FN1; the disease is laryngotracheoesophageal cleft.