Because experimenters in our study were blinded to genotype and evaluated sex and age-matched GPR55 KO and WT mice in multiple neuropathic (PSNL, paclitaxel-induced neuropathic pain) and inflammatory (formalin, capsaicin, CFA) pain states with multiple dependent measures (mechanical, cold and heat responsiveness) it is unlikely that obvious experimental confounds contribute to the pattern of results obtained here (i.e. preserved nociceptive responding in inflammatory and neuropathic pain states). The gene discussed is GPR55; the disease is neuropathic pain.