In summary, patients with CF and a G551D-CFTR mutation on ≥1 allele and receiving IVA in real-world settings reported better generic and disease-specific HRQoL, better school productivity, and better symptomatology than patients with CF who are homozygous for F508del-CFTR and receiving SOC (without LUM/IVA) in multiple domains. This evidence concerns the gene CFTR and cystic fibrosis.