Recently, it was reported that exendin-4, an analog of glucagon peptide-1 (GLP-1), could attenuate the production of excessive mucus by restoring the FOXA2 expression in COPD, CF-diseased cells, and mouse lungs infected by P. aeruginosa. It was found that exendin-4 triggered GLP-1R-dependent PKA and PPAR-γ activation, which in turn increased the expression of PTEN and PTP1B phosphatases. The gene discussed is GLP1R; the disease is chronic obstructive pulmonary disease.