On the contrary, LPA/LPAR1-induced vascular leak was the main attribute (together with fibroblast recruitment) of the observed protection from BLM-induced chronic pulmonary inflammation and fibrosis upon LPAR1 genetic deletion [20](where no inflammatory changes were observed, especially in early time points) or pharmacologic inhibition [19], further supporting a differential role of ATX/LPA in acute vs chronic inflammation. Here, LPAR1 is linked to fibrosis.