However, our data did not confirm overexpression of Oxymetazoline hydrochloride HMGCS2 in ER negative tumors at the protein level: the group of TNBCs displayed only,2% CGS 21680 positives for HMGCS2. IAC as defined by morphological criteria is often characterized by a specific hormone receptor signature: AR+/ER-/PR that has been proposed as a marker for apocrine�Ctype tumors by Tsutsumi and coauthors, who suggested to include androgen receptor to immunohistochemical criteria. The identification of differentially expressed proteins that characterize the progression from early benign apocrine lesions to invasive stages opens a window of opportunity for designing and testing new approaches for pharmacological intervention as, for example, 15-hydroxyprostaglandin dehydrogenase and 3-hydroxymethylglutaryl-CoA reductase are currently being targeted for chemoprevention strategies in various malignancies. HMGCS2 is one of the rate-limiting enzymes controlling generation and re-utilization of ketone bodies. Recently it was shown that ketone bodies support the driving of neoplastic growth which is often accompanied by starvation of all components of tumor environment and it has been speculated that ketone inhibitors can be designed as novel therapeutics to effectively treat advanced cancer patients. Consequently, HMGCS2, the enzymes associated with ketone body production and re-utilization, might be considered as new ����druggable���� targets for anticancer therapy. Our finding that IACs are characterized by an overexpression of HMGCS2, suggests that the patients diagnosed with apocrine carcinoma might benefit from therapy with HMGCS2 inhibitors. In addition, the high levels of AR expression in the IACs makes this receptor a promising anticancer therapeutic target for this type of breast cancer, but the ability to exploit AR for therapy remains to be challenging. Given that AR and HMGCS2 are both overexpressed in IAC, the use of the dual therapy targeting two parallel AR and HMGCS2 pathways may provide an additional benefit for therapeutic attack of breast apocrine carcinoma.