Recent investigations of the cellular and molecular mechanisms of pain provide new hopes for more effective treatments for
patients with chronic pain. At the molecular and genetic levels, new proteins and genes related to sensory sensation have been identified.
However, many of these new discoveries have not resulted in better and more effective treatments for chronic pain. This disconnect between
discovery and better treatment options is due, in part to the negative side effects associated with new treatment options, and also as
a result of the ineffectiveness of these new drugs for inhibiting chronic pain. In this review, I will explore this disconnect between discovery
and treatment, and propose that the failure of previous medicines can be due to their limited effects on injury-related plasticity,
and question the common misperception of seeking compounds for high efficacy before understanding basic mechanisms of the target
proteins in pain-related plasticity.