AKT1 and neoplasm: More recently, a study demonstrated that replacing the oncogenic PIK3CA(E545K) mutation with wild-type PIK3CA in MCF7 luminal breast cancer cells that are ER-positive in the context of AKT1(E17K) knock-in leads to increased transformation and xenograft tumor volume, demonstrating that AKT1(E17K) can function as an oncogene in the context of an ER-positive, luminal breast cancer [19].