Recent studies support a role of TRPV4 in inflammatory mediator-induced sensitization to osmotic and mechanical stimuli: 1) TRPV4 contributes to the enhanced nociceptive behaviors in response to mechanical and osmotic stimuli, produced by inflammation and peripheral neuropathy [4,8], 2) inflammatory mediators can engage TRPV4 in DRG neurons in vitro [9] and 3) hypotonic stimuli elicit action potentials in C-fibers, and in presence of inflammatory mediators, the number of action potentials significantly increases, as does the percentage of responsive fibers [7]. Here, TRPV4 is linked to peripheral neuropathy.