There is also plenty of evidence that endogenous H2S produced from l-cysteine by cystathionine-γ-lyase (CSE), an H2S-forming enzyme, contributes to the Cav3.2-dependent pain in various animal models for inflammatory and neuropathic somatic pain [17,27,28], as well as visceral pain associated with cystitis or pancreatitis [19,[29], [30], [31], [32]]. The gene discussed is CACNA1H; the disease is chronic cystitis.