In addition, although the role of SET in breast cancer remains mostly unknown, it has been described high SET levels and low PP2A activity in the MCF-7 cell line [16], and the work by Switzer et al. [17] showed that COG112-mediated SET inhibition in the MDA-MB-231 breast cancer cells reduced AKT signaling and cell proliferation, indicating that SET could serve as a novel therapeutic target in these cancers. This evidence concerns the gene AKT1 and breast cancer.