The ability of cancer cells to adopt new phenotypes without further DNA mutations is now well understood to substantially influence tumour behaviour. Such plasticity has long been observed in melanoma, where early studies identified transcriptomic and phenotypic states not linked to specific genetic lesions1. More recent evidence indicates that most tumours encompass a heterogeneous yet reproducible number of transcriptional states3,4. The extent to which tumour cells transition between states is an open area of investigation and has been hypothesized to be regulated by cues from the tumour microenvironment (TME).