These findings not only indicate that H2S, SP and TRPV1 interact to instigate neurogenic inflammation in sepsis through activation of the ERK-NF-κB pathway, but also added to the growing evidence about the involvement of ERK1/2 in regulating the activity of NF-κB [14], [15], and the potential association between H2S and ERK-NF-κB [18], [51], [52], [53]. The gene discussed is TRPV1; the disease is Sepsis.