The involvement of FFA2‐induced endogenous PYY and GLP‐1 release48 and inhibitory neuronal (FFA3) SCFA mechanisms potentially underpin clinical observations showing that an increase in dietary fiber or intracolonic delivery of propionate elevates postprandial PYY and GLP‐1 levels, reducing energy intake and longer term weight gain in overweight adults,6 and promoting energy metabolism.5 Based on these findings, we suggest that targeting FFA2 and FFA3 together may offer additional therapeutic potential for the treatment of obesity and type 2 diabetes. The gene discussed is GLP1R; the disease is obesity due to melanocortin 4 receptor deficiency.