Emerging evidence suggests that the alternative chloride channel SLC26A9 is a modulator of CFTR function and a potential candidate to circumvent the primary ion transport defect in several organs affected by CF including the lungs, the pancreas, and the gastro-intestinal tract independent of the CFTR genotype (Li et al., 2017; Gentzsch and Mall, 2018). Here, SLC26A9 is linked to cystic fibrosis.