Since acetic acid and butyric acid were the most abundant constituents of intestinal SCFAs in AF patients, these results initially indicated that GM-derived SCFAs disturbances in the gut contribute to AF occurrence and may be associated with enhanced circulating inflammation mediated by altered GPR43 and NLRP3 mRNA expression in peripheral blood leukocytes, which is potential therapeutic targets for AF. The gene discussed is FFAR2; the disease is atrial fibrillation.