Recent studies of CFTR sequence evolution [64], protein residue co-evolution and structure [65], selection for intronic regulatory sequences [33], inferences regarding CFTR channel gating [66], and characterization of the cystic fibrosis disease mutational spectrum [67] are predicated on a mechanism that treats CFTR exonic, intronic, synonymous, and non-synonymous SNP production as a random process. Here, CFTR is linked to cystic fibrosis.