The primary cholesterol metabolite activates the ER, subsequently increasing BC cellular proliferation and tumor growth.33 Cholesterol is also a precursor for biosynthesis of estrogen, which in high levels is considered to be a mammary gland carcinogen.14 Oxysterol derivatives of cholesterol, such as 27-hydroxycholesterol, act as endogenous ER modulators and have been associated with worse outcomes in females with low estrogen.15 Here, ESR1 is linked to neoplasm.