In contrast, acetate promotes glycolysis in Th17 cells via GPR43 signalling, potentially exacerbating inflammatory responses in RA; clinical studies show a positive correlation between serum acetate levels and the IL-17+CD4+ T cell ratio in RA patients, suggesting the acetate-GPR43 axis as a potential therapeutic target [35,37,38]. This evidence concerns the gene IL17A and rheumatoid arthritis.