Accordingly, we reported that a variety of HDACIs, including three FDA-approved HDACIs, suppress E2 levels by altering StAR acetylation patterns, expression, and activity, not only in hormone-sensitive MCF7 cells, but also in primary cultures of enriched mouse breast tumor epithelial cells [8,11,20], emphasizing the potential of StAR as a therapeutic target for the management of ER+ BC. The gene discussed is STAR; the disease is breast neoplasm.