Inhibition of LPA-mediated Heps-HSC crosstalk via genetic deletion of Enpp2 in Heps halted disease progression in that model [152]; in particular, circulatory and hepatic LPA along with liver fibrosis, infiltration of CD68+ macrophages, Gr-1+ monocytes and liver lipid deposition were decreased. Here, ENPP2 is linked to Hepatic fibrosis.