SCE treatment also decreased the levels of H3K4 trimethylation (H3K4me3) and H3K36 trimethylation (H3K36me3) at the Smad3 promoter and its transcription in cardiac fibroblasts, which contributed to the suppressed expression of fibrosis-related genes and the attenuated myocardial fibrosis in mice after MI. The gene discussed is SMAD3; the disease is myocardial infarction.