TKT and hepatocellular carcinoma: An adenovirus was created simultaneously expressing a trans-splicing ribozyme targeting hTERT and HSV-TK, along with a miR-122a recognition site, with the hypothesis that high miR-122a levels will lead to degradation of the ribozyme in normal hepatocytes, while low miR-122a levels in HCC cells will allow functioning of the ribozyme, causing degradation of hTERT, expression of HSV-TK, and cell death [33].