AKT1 and neoplasm: Both tumor types are inhibited by the antiprogestin MFP, but differ in their activation of PI3K/Akt pathway: C4-HI tumors display higher levels of PI3K/Akt, lower PTEN, and higher response to the PI3K inhibitor LY294002, or the mTOR inhibitor rapamycin, than to endocrine inhibitors, while C4-HD tumors are more responsive to endocrine inhibitors [27].