Our experiments indicated four important findings: (1) exogenous H2S significantly increased the expression of the three enzymes in vivo, (2) 25–100 μM NaHS pretreatment increased CBS levels in a concentration-dependent manner, and 50 μM NaHS treatment increased CSE/CBS activity in vitro, (3) endogenous H2S played an important role in protecting the ischaemic heart after MI, and (4) when CSE was either knocked down (in vitro) or knocked out (in vivo), the expressions of CBS and 3-MST increased due to compensation. The gene discussed is CBS; the disease is benign neoplasm.