MTOR and neoplasm: For example, a recent study using a reverse-pharmacology approach, which involved the expression of a rapamycin-insensitive form of mTOR in squamous cancer cells, showed that cancer cells are the primary targets of rapamycin in vivo, and that mTOR controls the expression of hypoxia-inducible factor-1α (HIF-1α), a key transcription factor that orchestrates the cellular response to hypoxic stress, including the regulation of the expression of angiogenic factors, thus providing a likely mechanism by which rapamycin exerts its tumor suppressive and antiangiogenic effects [13].