Cystic Fibrosis (CF) Treatment Market size was valued at USD 5040.0 million in 2021 and is expected to reach USD 9332.3 million by 2028, at a CAGR of 9.2% during the forecast period 2022-2028. Cystic fibrosis is a genetic disorder that causes severe damage to secretory glands of body such as lungs, pancreas, liver and intestines. It is more common in lungs. The disease is progressive with several mutations in the genes, which causes cystic fibrosis. In cystic fibrosis, the abnormal secretions from various secretory glands builds mucus which results in improper working of the organ that is affected. The treatment of cystic fibrosis helps loosening mucus which includes physical therapy. There are various therapeutic products available for the treatment of cystic fibrosis, which include enzymes, antibiotics and others. According to CFF’s national patient registry, the median age of the person with cystic fibrosis is currently 33.4 years. Basing on the severity of the disease, cystic fibrosis signs and symptoms vary. The Wide- research on Cystic Fibrosis (CF) resulted in dramatic improvements in the treatment of the disease, which has quadrupled the median life expectancy to 37 years of age in the U.S. In parts of the world where state-of-the-art medical care is not available, life expectancy remains much lower. In Europe, 51.8% were adults with age 18 years or more and 48.2% were less than 18 years old. New therapeutics are currently in development, of which some may provide a functional CFTR protein in patients with some versions of the gene, potentially eliminating many disease complications and allowing people with the disease to live essentially normal lives. Cystic fibrosis is a hereditary disease that mostly affects the lungs, but also affects the pancreas, liver, and kidney. The cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation causes it. This gene, which is found on chromosome 7, is in charge of perspiration, mucus, and bodily fluids regulation. However, a mutation in this gene causes CFTR activity to be absent, resulting in chloride loss and protein structural changes.