A faulty cystic fibrosis transmembrane conductor regulator gene causes the hereditary disease. This causes pulmonary symptoms and pancreatic insufficiency, malnutrition, liver illness, and CF-related diabetes. The assumption is fibrotic growth destroys islets. The article aims to review cystic fibrosis-related diabetes to cover previous findings, contemporary breakthroughs, and future research plans. We conducted a comprehensive literature survey on CFRD's clinical manifestations, monitoring, and analysis, as well as its diagnosis and management. A few theories, such as the deletion of phenylalanine at amino acid position 508, relate pancreatic dysfunction to cystic fibrosis. A study of 950 cord blood samples in India found 1:40000 CF newborns. Many groups and foundations recommend CF diabetic diagnosis criteria. They include oral glucose tolerance tests (OGTT), continuous glucose monitoring (CGM), HbA1c, and fasting hyperglycemia. Recently, fructosamine and glycated albumin have also used to diagnose hyperglycemia in Cystic fibrosis. The accuracy of OGTT and CGM makes them valuable diagnostic tools, with OGTT being the standard. CFRD causes pulmonary decline, malnutrition, microvascular issues, and death. Dietary control, which should be high in calories, protein, fat, salt, and carbohydrates, and physical activity are key CF treatments. Numerous pathophysiological pathways cause diabetes, however, insulin is still the best therapy. Drugs and tools are available to improve insulin treatment. Other therapies include metformin, repaglinide, GLP-1 agonists, and DPP-4 inhibitors.