CPT is a uniquely difficult condition, often associated with Neurofibromatosis (NF1), where bone healing is compromised. Although rare, the severity of this condition and the multiple procedures often entailed in treating it, warrant research attention. As study material is limited, animal models of the disorder are desirable for testing new treatments. We sought to create a model of CPT where both copies of the NF1 gene were ablated at the fracture site, as has been found in some clinical specimens. NF1 floxed mice had fracture surgery; both closed fracture and open osteotomy were performed. Either a Cre- or control GFP-adenovirus was injected into the fracture site at day zero. Recombination was confirmed in ZAP reporter mice. Additionally, cell culture studies were used to examine the possible responses of NF1+/+ (wild type) NF1+/− or NF1−/− to drugs which may rescue the dysregulated Ras/