CHI3L1 and cystic fibrosis: Based on previous studies, using a genetic brp-39 knock-out and a humanized YKL-40 transgenic overexpressing mouse, demonstrating that YKL-40/BRP-39 plays a role in tissue remodeling, cell death pathway regulation and airway obstruction [29],we speculate that released YKL-40 contributes to the cellular homeostasis and tissue remodeling, thereby modulating pulmonary function and inflammation in CF.