The data showing impaired insulin secretion in both primary human β-cells, andanimal models with the ∆F508 mutation seems to reflect the observed disturbedfirst-phase insulin release in CF and CFRD patients alike.8,17 Abnormaland impaired glucose tolerance is seen in CF patients as well.18,19Additionally, patients with CF have a skewed secretory ratio ofproinsulin:insulin,22,23 which could be attributedto the proposed role for CFTR in insulin granule priming. This evidence concerns the gene INS and cystic fibrosis.