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. The gene discussed is LPAR4; the disease is neoplasm.