**4. Animal models of cystic fibrosis**

Animal models serve an important testing ground for somatic cell gene transfer applications. Mice with null mutations [86-89], specific disease associated *CFTR* mutations [90-92], and conditional CFTR null alleles [93] have contributed to the understanding of molecular mechanisms of CF. However, mice do not recapitulate several aspects of CF lung disease pathogenesis. As discussed above, many studies evaluating integrating gene transfer vector delivery to the lungs of mice have been conducted. For these reasons, we now discuss efforts to deliver integrating vector to new animal models CF.

### **4.1. CF rat**

Tuggle and colleagues used zinc finger nucleases to disrupt CFTR exon 3 in rats [94]. CFTR-/ rats recapitulate many aspects of human disease including intestinal obstruction, obstruction of the vas deferens, and abnormalities in nasal mucus production. It is currently not clear if CFTR null rats develop lung disease. To date, no gene correction studies have been reported in this novel model.
