The induction of the glycolytic pathway we have documented in STS patients is likely to represent an adaptive consequence of hypoxic conditions, mediated by genomic alteration and/or expression of hypoxia inducible factors (HIF1A and HIF2A), which have been shown to induce glycolytic genes [18], and recently to play a fundamental role in the expansion and maintenance of the GBM stem cell compartment [19,20]. The gene discussed is EPAS1; the disease is glioblastoma.