Several instances have been described regarding the influence of multiple distal enhancers on gene expression, such as the well characterised locus-control-region (LCR) of the Beta-globin genes or the c-Myc enhancers active across multiple cancer types.45,58–60 Given the extensive interactions between this locus and its adjacent gene desert, we hypothesise that a consorted effort of multiple enhancers is responsible for the overexpression of these genes in cancer possibly driven by extensive binding and activity of ERα. The gene discussed is ESR1; the disease is cancer.