It has been suggested that increased activation of the mechanistic target of rapamycin (mTOR) pathway [11], possibly through the PI3K/Akt pathways, plays a role in endocrine resistance exhibited by some ERα + breast cancer cells, since inhibition of mTOR signaling with rapamycin could restore sensitivity to tamoxifen in laboratory models of resistance [12,13]. The gene discussed is ESR1; the disease is breast cancer.