Particularly the induction of HIF-1α, as a response to paracrine low oxygen pressure, allows the expression of genes promoting the reprogramming of tumor metabolism toward the glycolytic pathway, increasing glucose uptake, expression of glycolytic enzymes and lactate production, and regulating pyruvate metabolism in both hypoxic and normoxic (e.g., VHL deficient) cells [47, 156]. The gene discussed is HIF1A; the disease is neoplasm.