This study by Walter Kolch and colleagues indicates that mutant KRAS leads to the stabilization of p53 through the MST2–LATS1 kinase pathway, which results in apoptosis. This is counteracted through mutant KRAS activation of the epidermal growth factor receptor and the remaining wild-type KRAS allele, which inhibits the MST2 pathway through the activation of AKT. Consistently, there is a negative correlation in mouse and human colorectal tumours between mutant KRAS expression and MST2 expression, and tumours that express both have increased levels of apoptosis.