We described the effect of beinaglutide on inhibiting hyperinsulinemia, which was opposite to the effect of GLP-1RAs on β-cell function in patients with type 2 diabetes.[12] The patient showed a weak response of cortisol, IGF-1, and glucagon to hypoglycemia at baseline, which may attribute to recurrent hypoglycemia.[13] After 1-month beinaglutide treatment, the glucagon levels were not suppressed. The gene discussed is IGF1; the disease is hyperinsulinism.