This could account, for example, for the observed dysfunction of Rab27a in blood neutrophils from adult CF patients, a key protein involved in tertiary and secondary granule exocytosis, coupled with the finding that significant improvement in Rab27a function in these neutrophils can be brought upon by ex vivo treatment with the CFTR potentiator ivacaftor [98]. This evidence concerns the gene RAB27A and cystic fibrosis.