Importantly, the CFTR antibodies used in our experiments gave the predicted predominantly apical as well as cytoplasmic immunostaining pattern in pancreatic sections from control patients (Figs 2A, S1 and S2), or only cytoplasmic in the case of patients homozygous for the mutation F508del (ΔF508, Fig 2B) but did not generate an immunological signal in pancreas sections from a CF patient homozygous for the truncating CFTR mutation G542X (Fig 2C and 2D) leading to protein absence, or mice lacking Cftr expression (Fig 2E and 2F). The gene discussed is CFTR; the disease is cystic fibrosis.