Cystic fibrosis (CF) is a devastating disease cause by mutations (mistakes) in the gene coding for a protein named Cystic fibrosis transmembrane conductance regulator (CFTR). CF affects the function of many organs but the most frequent cause of death in most CF patients is lung failure. CF patients have thick mucus in their lungs which results in repeated lung infections. The damage caused by these infections causes lung failure and premature death around the age of 40. The goal of this project was to develop a  CRISPR/Cas9 based genome editing platform to correct genetic mutations that cause CF in airway basal stem cells. In working towards this aim, we used a two pronged strategy. We first developed methods to correct the F508del mutation that affects over 70% of patients in the US. We achieved >30% correction of the F508del mutation in airway stem cells. On differentiation, the corrected airway basal stem cells differentiated into epithelial sheets that showed 30-60% wild-type CFTR function. We further identified an FDA approved scaffold used for wound healing in sinonasal surgeries and embedded the corrected airway stem cells. The embedded cells retained expression of stem cell markers (cytokeratin 5, p63 and cytokeratin 14), differentiated when removed from the membrane and retained CFTR function.  We then adapted the platform to insert the full-length CFTR coding sequence to correct most CFTR mutations (Universal strategy). We tested this universal strategy in 10 CF samples and observed wild-type level restoration of CFTR function. This strategy will be especially of interest for treating patients with nonsense mutations who cannot be treated using current state of the art triple combination modulator therapy. Thus, we developed gene corrected cells that restore CFTR function when differentiated and can be embedded on a biodegradable scaffold. Future work will focus on optimization of transplanting the corrected cells in an animal model.