In this study, we found that both inhibitors blocked over 90% (93.9% by PAG and 96.7% by BCA) of all TNF-α-induced early H2S production, indicating that in colonocytes, CSE is responsible for most of the immediate increase in the endogenous H2S level after TNF-α stimulus, confirming earlier reports on animal models of colitis [38]. The gene discussed is CTH; the disease is colitis.