Importantly, both area at risk (control: 75.3 ± 3.4, GLP-1(9–36): 79.6 ± 0.4 %LV; n ≥ 5) and infarct size (control: 47.1 ± 4.6, exendin-4: 47.2 ± 1.2 %LV; n ≥ 5) were comparable between MI groups at 4 weeks (Fig. 1a–b), thereby facilitating specific investigation of direct effects on chronic remodelling. The gene discussed is GLP1R; the disease is myocardial infarction.