Additionally, since blockade of TRPV1 by capsazepine attenuated H2S-augmented COX-2 and PGEM response but had no effect on PAG-mediated attenuation of both parameters in septic lungs, we ascertained from our data that sepsis has a significant sensory neurogenic component that is mediated by H2S in a TRPV1-dependent manner, and that H2S stimulation of TRPV1 occurs upstream of COX-2 and PGEM in sepsis [83]. The gene discussed is TRPV1; the disease is Sepsis.