A recent study further supports this evidence, showing that CFTR inhibitors reduce, rather than completely inhibit, the overall secretory response in mouse, rat, and human beta cells, demonstrating that CFTR participates, at least in part, in the secretory response of beta cells, and intrinsic β-cell dysfunction may directly participate in the pathogenesis of CFRD [18]. This evidence concerns the gene CFTR and cystic fibrosis-related diabetes.