More recently, Boutin and coworkers, using an experimental mouse model in which mutations in APC, P53 and KRAS are spatially and temporally regulated, have shown that KRAS expression is required for tumor maintenance, even in a situation where KRAS activation is not an initiating event: loss of KRAS expression caused the apoptosis of primary and metastatic colon adenocarcinomas, while no apoptosis was induced in simple adenomas [133]. This evidence concerns the gene KRAS and neoplasm.