The excessive activation of HIF1α in cancer, despite oxygen availability, is often driven by oncogenes (e.g., ERBB2, PI3K, Ras, protein kinase B/AKT, mTOR) and mutations in tumour suppressors (e.g., Von Hippel–Lindau (VHL) and PTEN) [6,10]. This evidence concerns the gene AKT1 and neoplasm.