Overexpression of EZH2 promotes anchorage independent cell growth and invasion, which require an intact SET domain and HMT activity, and is correlated with accelerated proliferation and reduced differentiation in BC (Kleer et al., 2003; Raaphorst et al., 2003; Bachmann et al., 2006; Collett et al., 2006; Gong et al., 2011; Wu and Crowe, 2015; Granit et al., 2018). Here, EZH2 is linked to breast cancer.