New findings in Wnt1-driven mouse mammary tumours might explain the nonhierarchical evolution of tumours that result in cancers harbouring multiple genetically distinct subclones, rather than a single 'self-interested' dominant clone. Such tumours were found to comprise distinct basal and luminal cell subclones, and functional cooperation between both cell types was required for tumour growth when implanted into secondary recipient tumour-prone mice. Specifically, the viability of Hras-mutant basal subclones was reliant on paracrine interactions with Wnt1 produced by luminal Hras-wild-type subclones. Although Wnt1 activation and dependency is uncommon in human breast cancer, similar cooperative mechanisms might be involved in tumorigenesis.