Indeed, it is well established that ongoing endocrine treatment can induce adaptive changes in breast cancer cells resulting in an aberrant activation of growth factor-mediated proliferative and survival pathways such as PI3K (Phosphoinositide 3-Kinase) Akt/mTOR (mechanistic target of rapamycin) and Rat sarcoma viral oncogene (RAS)/Mitogen-activated kinase kinase (MEK)/MAPK which in turn are able to induce an estrogen-independent receptor activation [93]. The gene discussed is MTOR; the disease is breast cancer.