However, HIF1α is also often stabilized in cancers, including brain tumors 105, by other factors such as overexpression of pyruvate kinase isozymes M2 (PKM2), Ras, proto‐oncogene tyrosine‐protein kinase Src and ErbB2 and constitutive activation of the phosphatidylinositol‐4,5‐bisphosphate 3‐kinase (PI3k), protein kinase B (Akt) or mammalian target of rapamycin (mTOR) pathway 79, 83. This evidence concerns the gene HIF1A and cancer.