There is evidence that has indicated HIF-1α accumulation even under normoxic conditions in tumor cells after the loss of tumor suppressors such as von Hippel-Lindau (VHL) or Phosphatase and Tensin homolog (PTEN) or the activation of oncogenes such as Rat sarcoma (RAS), sarcoma (SRC), and phosphoinositide 3-kinase (PI3K) [34,39]. The gene discussed is HIF1A; the disease is neoplasm.