However, both activation of JNK and repression of Nf-κB have been linked to p75NTR-mediated hyperalgesia [26], and the overexpression of TRPV1 in DRGs after NGF-mediated activation of p38 has been indicated as a cause of inflammation-induced neuropathy and as a possible cause of neuronal distress provoked by the intracellular Ca2+ overload mediated by TRPV1 [8, 30]. Here, NGFR is linked to neuropathy.