Consistently, NaHS treatment has been reported to activate an endogenous angiogenic agent VEGF by elevating CSE levels, resulting in the inhibition of anti-angiogenic factors such as angiostatin, endostatin, and patatin and, subsequently, the formation of new blood vessels in the heart and reduction in the infarct area in myocardial infarction (MI) in mice [71]. The gene discussed is COL18A1; the disease is myocardial infarction.