In a model of atherosclerosis, lack of H2S-generating enzyme CSE, or H2S donor administration, have been shown to induce SIRT1 expression and increase deacetylation activity by sulfhydration of two CXXC domains, which caused SIRT1 to bind more zinc, therefore promoting its activity, and decreasing its ubiquitin-dependent degradation [30]. The gene discussed is SIRT1; the disease is atherosclerosis.