Chronic pathological pain is characterized by extensive plasticity of the systems involved in pain signal transmission and modulation and tissue remodeling in several CNS structures. These long-lasting alterations are mediated by, or associated with, changes in the production of key molecules of nociceptive processing. Gene-based approaches offer the unique possibility of using local or even cell-type specific interventions to correct the abnormal production of some of these proteins, modulate the activity of signal transduction pathways, or overproduce various therapeutic secreted proteins. We showed that certain viral-derived vectors are particularly suitable for mediating gene transfer highly preferential for instance into the primary sensory neurons or into the spinal cord glial cells that represent particularly pertinent targets in the search for new therapeutic strategies of pathological pain.