In breast cancer cell lines that are initially sensitive to PI3K or Akt inhibitors and that express low levels of SGK1, prolonged treatment with PI3K or Akt inhibitors resulted in up-regulation and activation of SGK3 that also substituted for Akt by phosphorylating TSC2 and ultimately activating mTORC1 [12]. The gene discussed is AKT1; the disease is breast carcinoma.