While it increases the abundance of HCV RNA in HCV infection by binding directly to the 5’-UTR of the viral genome, it decreases HBV replication through an inhibitory effect of p53 on HBV transcription, and consequently it acts as a tumor-suppressor through both decreasing of HBV replication and directly targeting cyclin-G1, as well as Wnt/β-catenin, and NDRG3 pathways. This evidence concerns the gene CCNG1 and neoplasm.