The notion that 1-EBIO acted as a CFTR Cl− channel opener in the absence of cAMP-mediated activation was supported by the observations i) that 1-EBIO-induced Cl− secretory responses were inhibited by the CFTR inhibitor CFTRinh-172, and ii) that 1-EBIO failed to induce Cl− secretion in rectal epithelia from CF patients carrying two severe CFTR mutations that caused a lack of functional CFTR Cl− channels in the apical cell membrane (Table 1) [7], [17]. This evidence concerns the gene CFTR and cystic fibrosis.