Furthermore, high CTGF expression was significantly correlated with poor clinicopathological features in HCC patients.<h4>Conclusion</h4>Our findings revealed that CTGF derived from CAF-EVs promoted the proliferation and invasion of HCC cells via activation of the Notch1/Snail1 pathway, highlighting CTGF derived from CAF-EVs as a prognostic biomarker and therapeutic target in HCC. The gene discussed is SNAI1; the disease is hepatocellular carcinoma.