This disruption leads to HIF-1α stabilization and activation independent of PHD, even under normoxic conditions [51]. Taken together, these findings suggest that the downstream effects of the PI3K/AKT/GSK3 pathway may involve FoxK1 or other coexisting transcription factors that facilitate HIF-1α transcription [51], and further investigations are needed to explore these signaling pathways in cancer cells. The gene discussed is AKT1; the disease is cancer.