Noteworthily, systemic levels of ATX/LPA in the same mouse strains have been shown not to affect the pathogenesis of other modelled chronic inflammatory diseases, such as rheumatoid arthritis [28], pulmonary fibrosis [35] and liver fibrosis (with the exception, as expected, of liver fibrosis that was found exaggerated in the transgenic TgEnpp2+/+ mouse that express ATX driven from the liver specific a1t1 promoter)[27] highlighting the importance of local ATX expression in chronic inflammation. Here, ENPP2 is linked to pulmonary fibrosis.