SLC26A6 and cystic fibrosis: In an attempt to identify the mechanisms responsible for the defect in HCO3− transport in CF, it was shown that CFTR could upregulate SLC26A3 and SLC26A6 expression in cultured pancreatic duct cells [30] as well as stimulate their activity [31], thus providing a first indication of the potential cross-talk between CFTR and SLC26 family members.