While single-agent anti-EGFR therapy may not increase patient survival in all cancer types [60], promising alternative (or adjunct) targeting approaches include regulating AREG release by ADAM-17 inhibition [61], immunological blockade of AREG [55], or disrupting the AREG feedback loop through combined inhibition of YB-1 and mTOR (downstream of PI3K) [62]. The gene discussed is MTOR; the disease is cancer.