A compromised function of the SLC26 family members is associated with the primary defect of cystic fibrosis (CF [MIM: 219700])—impaired Cl− absorption in conjunction with aberrant HCO3− and fluid secretion—through the inability of CFTR mutants to activate the Cl−/HCO3− exchange mediated by the SLC26 family members, most notably SLC26A3 and/or SLC26A614,15,24–27. The gene discussed is CFTR; the disease is cystic fibrosis.