As incretin axis dysfunction is thought to contribute to the development of glucose intolerance in CF [17], incretin therapy, specifically using dipeptidyl peptidase 4 inhibitors (DPP4i), which stimulate insulin secretion and suppress glucagon secretion in a glucose-dependent way, could be a good alternative in the early stages of CFRD. The gene discussed is DPP4; the disease is cystic fibrosis-related diabetes.