However, EZH2 overexpression is rarely accompanied by a matched increase in global H3K27me3 levels, and in fact, evidence from genetic studies in both mouse and human systems suggests that EZH2 upregulation in cancer may be a response to cell proliferation and the need to compensate for cell division‐induced dilution of H3K27me3 66, 67, 68, 69. Here, EZH2 is linked to cancer.