A key dilemma in embryonal rhabdomyosarcoma is that YAP is expressed, nuclear and presumably active in the majority of human ERMS cases7 but that YAP1 is not significantly mutated in human ERMS which has a high frequency of oncogenic RAS mutations1 Given that interactions between mutated, oncogenic RAS and YAP have been reported for other cell and cancer types13–15, we tested for evidence that mutated, oncogenic KRAS can activate YAP in (rhabdo-) myoblasts to regulate the expression of a shared set of genes. Here, KRAS is linked to cancer.