We propose that the post-menopausal hormonal milieu and subsequent intratumoral E1 levels, are associated with a pro-inflammatory phenotype in ER+/HER2- BC, characterised by increased TNFα and NFκB expression, which work in tandem to downregulate PEDF expression, thus increasing BC metastatic potential as PEDF’s control over pro-metastatic mediators is lost. The gene discussed is ERBB2; the disease is breast cancer.