Inflammation represents the body's natural response to tissue damage; however, 
chronic inflammation may activate cell proliferation and induce deregulation of 
cell death in affected tissues. Chronic inflammation is an important factor in 
the development of hepatocellular carcinoma (HCC), although the precise 
underlying mechanism remains unknown. Epigenetic events, which are considered 
key mechanisms in the regulation of gene activity states, are also commonly 
deregulated in HCC. Here, we review the evidence that chronic inflammation might 
deregulate epigenetic processes, thus promoting oncogenic transformation, and we 
propose a working hypothesis that epigenetic deregulation is an underlying 
mechanism by which inflammation might promote HCC development. In this scenario, 
different components of the inflammatory response might directly and indirectly 
induce changes in epigenetic machineries ('epigenetic switch'), including those 
involved in setting and propagating normal patterns of DNA methylation, histone 
modifications and non-coding RNAs in hepatocytes. We discuss the possibility 
that self-reinforcing cross-talk between inflammation and epigenetic mechanisms 
might amplify inflammatory signals and maintain a chronic state of inflammation 
culminating in cancer development. The potential role of inflammation-epigenome 
interactions in the emergence and maintenance of cancer stem cells is also 
discussed.