HIF-1α expression may be increased via loss-of-function mutations of tumor-suppressor genes or gain-of-function mutations of oncogenes, and activation of the Phosphoinositide 3-kinase/Akt/Mammalian Target of Rapamycin (PI3K/Akt/mTOR) and Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase (MAPK/ERK) pathways [39]. The gene discussed is MTOR; the disease is neoplasm.