The primary vascular ECs of WT and Lpar2−/− mice were separated, and the results of studies in vitro showed that cell activity of Lpar2−/− mice ECs decreased more under injury conditions (Figure 2e), suggesting that the loss of Lpar2 may affect the activity and function of ECs, lead to enhanced vascular permeability (Figure 2f), and increase the production of DVT. Here, LPAR2 is linked to deep vein thrombosis.