In 2013, Schwank et al. used the CRISPR–Cas9 genome-editing system to correct the site of the CF transmembrane conductor receptor (CFTR) through homologous recombination in CF patient-derived intestinal and colonic organoids, and this provided a theoretical basis for gene correction by homologous recombination in primary ASCs from patients with single-gene hereditary defects (Schwank et al., 2013). This evidence concerns the gene CFTR and cystic fibrosis.