Furthermore, the authors speculated that HIF-1α promoted stem cell enrichment, in part, through the Akt/β-catenin pathway, which was reported to be a key regulator of CSC self-renewal in breast cancer, because HIF-1α increased levels of both phospho-Akt and phospho-S552 -β-catenin in SUM159 cells, and β-catenin was inactivated (not phosphorylated) when HIF-1α was knocked down (81, 82). The gene discussed is AKT1; the disease is breast cancer.