Peripheral inhibition of CaV2.2 by ω-CgTx-MVIIA has been reported previously to attenuate mechanical hypersensitivity in a peripheral nerve injury model of chronic pain (White and Cousins, 1998), suggesting that in addition to a role in transient heat hypersensitivity, peripheral CaV2.2 channels may also contribute to a positive feedback cycle of ongoing local release of pro-inflammatory mediators and nociceptor depolarization in chronic inflammation (Fig. 7). This evidence concerns the gene CACNA1B and peripheral nerve injury.