The activity of primary sensory neurons is critical for the development and maintenance of persistent pain states. Following peripheral injury, primary sensory neurons show complex activity-dependent plasticity as a result of prolonged noxious stimuli and ectopic discharges. This altered activity in the primary sensory neurons is transmitted to spinal dorsal horn neurons and ultimately to the brain which results in persistent pain in a proportion of patients. While genetic studies have advanced our knowledge of nociceptive pathways, our current understanding does not explain variations in the susceptibility of individuals to the development of this cancer-related persistent pain. Common genetic variations in pain phenotypes show inconsistencies across studies6 and have not facilitated the development of new treatments. Epigenetic variations within the genome are known to cause misregulation of protein at a cellular level which may modulate nociception. My long term goal is to determine the contribution of epigenetic pathways to enhanced pain sensitivity and the establishment of cancer-related persistent pain. Specific research questions that I am eager to explore include (1) the association between altered chromatin structure in the dorsal root ganglion and cancer-related pain, and (2) cell-type specific changes in chromatin accessibility associated with chemotherapy-induced peripheral neuropathy.