Importantly, normal SVZ cells responded in a different way; indeed, by chemically stabilizing HIF-1α, REDD1 was transiently upregulated and Akt/mTOR pathway was not inhibited, unlike in tumor cells, following exposure to high oxygen tension (Figure 3H), and Akt and Stat3 were eventually upregulated by CoCl2. The gene discussed is AKT1; the disease is neoplasm.