DUSP1 and neuropathic pain: We demonstrated that MKP-1 retains its substrate specificity, namely p-p38, in spinal cord (as also observed in other systems) and that dephosphorylation of p-p38 may explain the reduction of spinal pro-algesic factors (cytokines and chemokines) and mechanical hypersensitivity in a rat model of neuropathic pain.