Inflammation plays a central role in the manner that the nervous system responds to injury. These effects include vasodilatation, increased vascular permeability, plasma extravasation, cell migration, and pain. Extracellular signals associated with inflammation may also lead to increased levels of pro-nociceptive chemokines/receptors that directly contribute to persistent or chronic pain behavior. To date, research focused on improving the treatment of chronic pain has largely ignored the role of inflammation-associated transcription factors such as nuclear transcription factor in activated T cells (NFAT). Herein we discuss the idea that activation of this transcription factor may be responsible for the production of chemokines receptors in both neuronal and non-neuronal cells of the peripheral nervous system. Taken together, a better understanding of the transcription of these pro-nociceptive genes may lead to the development of novel analgesic targets.