Sanz et al. explored CRISPR/Cas9-based methods to edit specific CF-causing mutations: c.3140-26A>G, c.1679+1634A>G, and c.3718-2477C>T CF, achieving successful excision through the non-homologous end joining (NHEJ) pathway in a significant proportion of transfected cells [181]. This evidence concerns the gene CFTR and cystic fibrosis.