Given that ESR1-enhancer hypermethylation is prevalent in acquired endocrine resistance in vitro (Figs 1e and 2a-d) and in molecular subclassifications of breast cancer that are intrinsically less responsive to endocrine therapy (Fig. 3a–c), we next sought to determine the methylation status of a panel of these loci in ESR1-positive (luminal A) breast cancer samples from patients with different outcomes. The gene discussed is ESR1; the disease is breast cancer.