In a similar strategy to the reprogramming of somatic cells into pluripotent stem cells using a set of four master TFs,56 the simultaneous overexpression of SOX2, OLIG2, POU3F2, and SALL2 reprograms differentiated GBM cells into CSC able to drive tumor formation.16 Likewise, glioma-initiating cells can be obtained from tumor suppressor-deficient astrocytes through the ectopic expression of SOX2, OLIG2, and ZEB1. 57 EZH2 is the catalytic unit of the PRC2 and is overexpressed in GBM. This evidence concerns the gene SALL2 and neoplasm.