Approximately two-thirds of breast cancers are ERα-positive and will potentially respond well to anti-estrogens.29,43 SETD7-driven methylation at ERα-K302 positively affects the stability of the ERα protein and transcriptional efficiency of the ERα gene.29 SETD7 knockdown leads to a twofold decrease of the ERα half-life, and K302 methylation stabilizes ERα, possibly by preventing the ubiquitination of K302 or by promoting the ERα–calmodulin interaction. Here, ESR1 is linked to breast cancer.