In addition, mutations in the MUC5B gene, which encodes a mucin required for normal macrophage function and effective muco-ciliary clearance of bacteria in mice [7], is associated with an increased risk of developing both familiar and sporadic IPF [8], suggesting that bacteria may act as a cofactor in fibrosis initiation in genetically predisposed individuals. Here, MUC5B is linked to idiopathic pulmonary fibrosis.