Chitinases function as effector molecules and mediate airway inflammation in both human epithelial cells [1] and in mouse models of asthma [2], [3]; however, despite the lack of enzymatic properties, YKL-40 levels are elevated in serum and in the lungs of patients with asthma where they correlate positively with the severity of the disease and inversely with lung function [4] indicating a participation of YKL-40 in the activity level and/or the pathogenesis of the disease. Here, CHI3L1 is linked to asthma.