Neuropathic pain is experienced as a result of disease or physical injury affecting the somatosensory system. It can be associated with abnormal sensations (dysesthesia) or evoked by normally nonpainful stimuli. Glia has emerged as key regulators of neuropathic pain perception and potential targets for drug development. Glia are activated upon peripheral nerve damage and secrete a number of proinflammatory factors. This process involves many mechanisms including neuroinflammation, ion channel activation, and ligand-receptor interactions. This review describes recent advances in the understanding of neuropathic pain, including the role of glia and their targeting by current treatment approaches.