Furthermore, the involvement of TRPV4 in nociception is modified by multiple pro-nociceptive factors, including the prostanoid PGE2, the activation of protease-activated receptors PAR-2 signaling, inflammatory mediators, and nerve injury, all of which have been confirmed to increase TRPV4-dependent pain signaling in several physiological systems [73,74,78,81,82,83]. The gene discussed is TRPV4; the disease is injury.