Our data provide a proof-of-concept that pharmacological co-activation of basolateral KCNN4 K+ channels substantially potentiates residual CFTR function in native CF tissues (Fig. 4,5), and may thus provide an opportunity to improve therapeutic effects of current CFTR potentiator and corrector compounds developed either to improve the open probability (PO) or to increase the number of mutant CFTR Cl− channels in the apical cell membrane [10], [46], [47]. The gene discussed is KCNN4; the disease is cystic fibrosis.