Activation of ileal HIF-1α and VEGF signaling by HA35 correlates with similar processes in cancer biology, where overproduction of HA generates a positive feedback loop of increased metabolic demands, a shift toward glycolysis and PI3K/Akt-mediated glucose uptake, activation of HIF-1α, and a boost in endogenous HA synthesis [57,77,78]. The gene discussed is AKT1; the disease is cancer.