These previous studies demonstrated that SOX4 expression is increased in basal-like breast tumors with high PI3K activity, independent of genomic alteration in commonly altered PI3K/Akt regulatory genes including PIK3CA and PTEN, and that siRNA-mediated silencing of SOX4 abrogates the activation of this pathway in basal-like cell lines; however, the mechanism(s) by which SOX4 regulates this pathway in TNBC remains unknown. Here, AKT1 is linked to breast neoplasm.