While PRC2 function has predominantly been framed in the context of its histone methyltransferase activity, some studies have demonstrated the ability of PRC2 to methylate non-histone protein targets or for Ezh2 to modulate transcription independently of PRC2 in a cancer context31–33, including in a transgenic model of HER2+ breast cancer where exogenous expression of Ezh2 enhanced the capacity of tumour-initiating cells in a PRC2-independent fashion34. This evidence concerns the gene EZH2 and breast cancer.