For instance, it has been reported that targeted pseudouridylation converting UAA, UAG, or UGA to ΨAA, ΨAG, or ΨGA, respectively, in the context of disease genes, including β-globin (β-thalassemia), CFTR (cystic fibrosis), IDUA (Hurler syndrome), TP53 (cancer), and NF1 (neurofibromatosis type 1), resulted in both NMD suppression and PTC readthrough [114]. The gene discussed is CFTR; the disease is cystic fibrosis.