Other studies have demonstrated a critical role for Wnt signalling in the production and persistence of neuropathic pain after nerve injury and bone cancer.40 Rodent models show that in nerve injury and bone cancer pain models, respectively, Wnt signalling is activated, which may contribute to pain by regulating pro-inflammatory cytokines interleukin-18 and tumour necrosis factor-alpha, as well as NR2B and subsequent Ca2+-dependent signals in the dorsal horn. This evidence concerns the gene GRIN2B and injury.