Consistent with this hypothesis, we found that in the proneural subset there was a 75% of negative concordance (r = -0.44; p = 0.03) between PATZ1 and CXCR4, whose overexpression is an outcome common to multiple mechanisms of Epithelial-Mesenchymal Transition (EMT) induction in GBM and directly involved in determining the EMT phenotype [40]. The gene discussed is PATZ1; the disease is glioblastoma.