In this context, the negative impact of the common CFTR mutation F508del present on at least one allele in ∼90% of CF patients on SLC26A9 trafficking indicates that an ideal SLC26A9 modulator compound should overcome this interaction and facilitate trafficking of SLC26A9 from the ER to the plasma membrane independent of CFTR co-trafficking (Strug et al., 2016; Bertrand et al., 2017; Figure 2D). The gene discussed is CFTR; the disease is cystic fibrosis.