In the United States, chronic pain is a significant public health problem that affects over 100 million people and produces an estimated annual cost of about $635 billion. While the exact mechanisms that sustain differences in pain experiences remain mostly unknown, it is now widely agreed that chronic pain is caused and maintained by molecular, physiologic, and psychosocial factor. One mechanism by which psychosocial or environmental factors may influence pain perception, and severity is known as epigenomics. Unlike the genome that is determined at conception and remains constant throughout life, the epigenome is dynamic and subject to change over the lifespan of an individual. Studies on epigenetics and pain are relatively in its infancy. Few studies have described epigenetic changes in acute to chronic pain transition, visceral, neuropathic, and somatic chronic pain. An understanding of epigenetic mechanisms and their role in pain would place CRNAs on the cutting edge of precision health care. The purpose of this presentation is to discuss a mechanism by which life experiences could influence the development of chronic pain. To achieve this premise, first, I will present an overview of the two main types of epigenetic mechanisms. Second, I will explain how environmental factors such as chronic stress could induce epigenetic changes that cause and sustain chronic pain. Finally, I will summarize current knowledge of epigenetic changes in neuropathic, somatic, and visceral chronic pain, with implications for novel therapeutic interventions.