This approach was selected since K-rastmΔ4A/tmΔ4A mice are healthy [16,18], intestinal tumours in Min mice do not harbour K-ras activating mutations [20], and K-Ras 4A deficiency does not affect K-ras 4B expression in the small intestine [16] where, importantly, most (> 95%) intestinal tumours form in Min mice [reviewed [19]]. This evidence concerns the gene KRAS and intestinal neoplasm.