Although there were two potential GLI1 binding sites found in the promoter of Cav-1 with low homology to the canonical GLI1 binding sequence and Cav-1 luciferase reporter assay in this study also showed that forced expression of GLI1 leaded to up-regulation of Cav-1 promoter activity, we failed to prove the direct regulatory function of GLI1 on Cav-1 expression in HCC cells by ChIP assay. The gene discussed is GLI1; the disease is hepatocellular carcinoma.