Using mouse intestinal tumor cells that carry quadruple driver mutations for Apc, Kras, Tgfbr2, and Trp53, we showed that cells remained sensitive to anoikis if their Trp53 status was heterozygous, and a loss of wild-type Trp53 by LOH is necessary for the cells to survive in a dormant state and proliferate toward metastasis. Here, KRAS is linked to intestinal neoplasm.