CS-related TLR4 signaling was shown to increase MMP-1, a crucial actor in emphysema, in a MyD88- and IRAK1-dependent manner (Geraghty et al., 2011), while CS-exposed TLR4–/– mice were protected from emphysema, impaired lung function, airway fibrosis, and collagen deposition in small airways as compared with wild-type mice. This evidence concerns the gene MYD88 and pulmonary emphysema.