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. The gene discussed is SALL2; the disease is central nervous system cancer.