We investigated gene expression in the premalignant progression of dysplastic polyps in pigs carrying an engineered translational stop signal at codon 1311 in the APC gene (APC1311) orthologous to a human APC1309 mutation responsible for FAP5, to determine if molecular changes in the pig model parallel events in small polyps in humans, and whether pigs can be used to reveal new events in early CRC development. The gene discussed is APC; the disease is colorectal carcinoma.