Cystic fibrosis (CF) is a lethal disorder caused by mutations in the CFTR gene. CF causes severe and progressive lung disease characterized by persistent bacterial infections and bronchiectasis and affects roughly 1 in 2,000 people of European ancestry. My thesis work aims to identify small molecules that restore function to the mutant CFTR protein and to better characterize genes that interact with CFTR during its biogenesis. These CFTR genes could serve as therapeutic targets.