Demonstration of its role as a disease modifier, as well as overlapping expression of SLC26A9 and CFTR in several affected organs, suggest SLC26A9 as an attractive alternative therapeutic target to bypass the primary ion transport defect in CF (Sun et al., 2012; Blackman et al., 2013; Miller et al., 2015; Strug et al., 2016). Here, SLC26A9 is linked to cystic fibrosis.