Different groups were tracked to provide survival times that could be compared statistically to determine if the treatments had an effect on the length of time between induction of C-MYC expression in the liver and sacrifice due to tumor burden, a time frame defined in this study as “tumor latency.” We hypothesized that since φC31 integrase is associated with chromosomal aberrations in tissue culture, its expression might decrease tumor latency in these tumor-prone mice. The gene discussed is MYC; the disease is neoplasm.