Increasing evidence suggests that, upon stimulation by growth factors, phosphatidyl inositol-4,5-bisphosphate-3-kinase (PI3K) can upregulate the expression of HIF-1α through the activation of protein kinase B (Akt) and the mammalian target of rapamycin (mTOR), a serine/threonine kinase downstream of Akt, in various human cancers [27]. This evidence concerns the gene HIF1A and cancer.