CFTR modulator therapy has successfully restored near-normal chloride channel function in cells carrying the F508del mutation, which accounts for approximately 70% of cystic fibrosis cases worldwide. The treatment appears to correct the protein folding defect that prevents the mutated CFTR channel from reaching the cell surface and functioning properly. This represents a significant advance in precision medicine for cystic fibrosis, potentially transforming outcomes for the largest subset of patients with this progressive genetic disorder. The restoration of chloride transport could dramatically reduce the thick mucus accumulation that characterizes CF, leading to fewer lung infections and improved digestive function. While previous therapies have provided modest benefits, this level of functional restoration approaches what researchers have long considered the therapeutic threshold for meaningful clinical improvement. The success with F508del mutations could accelerate development of similar approaches for rarer CF variants, bringing personalized treatments closer to the remaining 30% of patients whose mutations have proven more challenging to target pharmaceutically.