Furthermore, PPT-A gene deletion and prophylactic treatment with SP inhibitor (L703606) shows that SP interacts with H2S and plays an important role in the pro-inflammatory effects of H2S. Moreover, H2S triggers systemic inflammation and multiple organ dysfunction in sepsis through transient TRPV-1 (transient receptor potential vanilloid-1)-mediated neurogenic inflammation [103]. The gene discussed is TRPV1; the disease is Sepsis.