Subsequently, taking the advantage of using the tachykinin precursor 1 gene (the gene that encodes substance P)-deficient mice, as well as using inhibitors of tachykinin receptor 1, the functional receptor of substance P and transient receptor potential vanilloid type 1 (TRPV1), we found that in mice with CLP-induced polymicrobial sepsis, TRPV1-mediated priming of the substance P-tachykinin receptor 1 axis was involved in H2S-induced activation of the ERK/NF-κB pathway and further resulted in sepsis-associated alterations, including systemic inflammation and organ injury [139,140,141]. Here, NFKB1 is linked to Sepsis.