To address the role of sPLA2-III in colon cancer further, we crossed Pla2g3−/− mice with ApcMin/+ mice, a model of human familial adenomatous polyposis in which the oncogenic Wnt/β-catenin signal is hyperactivated due to a mutation in the Apc gene, leading to spontaneous development of intestinal cancer, particularly in the small intestine48. This evidence concerns the gene APC and intestinal cancer.