Molecular processes facilitating tumor survival and spread such as deficiency or mutation of tumor suppressor genes (Von Hippel-Lindau, p53, and phosphatase and tensin homolog), and amplification of oncogenes (Akt, Ras) were shown to be associated with HIF-1α overexpression in previous studies (Munipalle et al., 2011). Here, HIF1A is linked to neoplasm.