Unfortunately, PI3K and mammalian or mechanistic target of rapamycin (mTOR) inhibitors have been shown to increase the expression of active phosphorylated extracellular signal-related kinase (p-ERK) and phosphorylated protein kinase B (p-AKT) in in vitro and in vivo ovarian cancer cell models, indicating that cancer cells have or develop resistance mechanisms to these inhibitors, likely through the loss of negative feedback loops [22,27,28,29]. The gene discussed is AKT1; the disease is ovarian carcinoma.