Cystic fibrosis is the most common life-threatening inherited disease in the UK. We study the protein whose dysfunction causes cystic fibrosis, CFTR. This same protein is responsible for the excessive salt/water loss occurring during secretory diarrhoeas (e.g. cholera). CFTR belongs to the superfamily of ABC proteins, which couple hydrolytic cycles at conserved nucleotide-binding domains (NBDs) to diverse cellular functions. CFTR is unique among ABC proteins in that its transmembrane domains comprise an ion channel. With our experiments we aim at deepening our understanding of  how CFTR works, setting foundations for pharmacological alteration of its activity.