In addition, we propose a potential mechanism for this resistance via Olig2 expression in Sox2+ SHH-MB cells, which has shown to acetylate and suppress p53 as well as inhibit p21 expression.31,32 Second, using the apoptosis-defective p53R172P mutant allele, we show that Sox2+ cells were resistant to p53-dependent p21-mediated cell-cycle arrest response, whereas radiation-enhanced p53R172P activation induced massive neuronal differentiation of Sox2− bulk tumor cells and drove them out of the tumor bed. The gene discussed is OLIG2; the disease is neoplasm.