Genome replication of the human hepatitis B virus (HBV) has been elucidated in great details at the molecular level. However, due to the lack of an in vitro infection system and a simple animal model, several steps of the virus life cycle have so far escaped to our understanding. The genomes of the mammalian hepadnavirus contain a unique regulatory gene, termed X. Whereas it is established that the X gene is required for a productive infection in mammalian hepadnaviruses, the exact function of the X protein in the viral life cycle remains unknown. In transient transfection studies, X protein has been shown to trans-activate a wide variety of promoters and to promote apoptosis. The molecular mechanisms underlying these activities are however unclear. For the last 5 years, conflicting data have suggested that X may possess cytoplasmic and nuclear activities interfering with signal transduction pathways and transcriptional machinery respectively. In this review, we will first focus on the viral life cycle of HBV, and will attempt to integrate the data reported by several groups including ours to speculate about step of virus life cycle that X is likely to regulate.