Another study reported that the splicing defect induced by the c.3718−2477C>T (3849+10kbC>T) and c.3140−26A>G CFTR mutations can be efficiently and precisely corrected using the AsCas12a nuclease in CF patient-derived intestinal organoids [93], thus offering a new alternative for CF therapy. The gene discussed is CFTR; the disease is cystic fibrosis.