This lack of correlation may be explained by: (a) secondary or modifier genes that protect or fail to protect an individual from CF lung and airways disease progression[7]; (b) additional genes that cause predisposition to CF lung and airways disease progression[7,8]; and/or (c) CFTR’s known role as a regulator of other conductances and cellular processes[4]. The gene discussed is CFTR; the disease is cystic fibrosis.