Similar enhancement of transcriptional activity was observed in other AFP-positive cells (Huh7 and Hep3B) treated with dAd/Ha2bm-GFP, demonstrating that deletion of the endogenous silencer domains can greatly augment the transcriptional activity of the AFP promoter without harming the promoter’s specificity toward AFP-positive HCC. Here, AFP is linked to hepatocellular carcinoma.