While this hypothesis remains to be directly tested in HLFs, it is possible that this could be an important mechanism for the establishment of pro-inflammatory or “pathological” HA matrices that promote lung inflammation given the elegant series of studies that have implicated TSG-6 as an important mediator of inflammation and airway hyperresponsiveness in asthma (15, 31, 42–44). This evidence concerns the gene TNFAIP6 and asthma.