The individual pancreatic cancer cell enhanced production of ECM and adapted to isolated stress by increasing expression of the stress-responsive gene lysophosphatidic acid receptor 4 (LPAR4) and promoted the production of fibronectin-rich ECM, which could compensate for the absence of stromal-derived factors and help tumor initiation.318 Furthermore, the ECM could also support neighboring cells without upregulated expression of LPAR4 through integrins α5β1 or αVβ3.318. Here, LPAR4 is linked to pancreatic neoplasm.