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work using human patients and genetically altered mice has identified some modifier genes and have advanced our understanding of CF pathophysiology [4]. In one study using CF mice on different genetic backgrounds, a region on mouse chromosome 7 was shown to ameliorate intestinal blockage and the effect was in part due to a calcium-regulated Cl-channel which compensated for loss of CFTR function [16,17]. Marker haplotypes of the syntenic region of human chromosome 19q13 were also shown to be associated with the risk of MI in CF patients [18]. In other work, a region on mouse chr. 6 was strongly associated with lung inflammation, consisting of mononuclear cell interstitial infiltration and fibrosis in CF mouse airways; and other loci on chr. 1, 2, 10, and 17 were also linked to the airway phenotype [19]."}

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