mTORC1 inhibitors generally have a cytostatic effect on ER+ breast cancer cells [13, 14], which is thought to be due in part to a loss of negative feedback signaling to activators upstream of PI3K including RTKs and IRS-1 [18–21], driving activation of PI3K/AKT to promote cell survival. The gene discussed is AKT1; the disease is breast carcinoma.