TP53 and glioma: On the other hand, impairment of mitochondrial metabolism via inhibition of complex I or loss of mitochondrial DNA leads to genetic inactivation of p53 and to a glycolytic switch in neural progenitor/stem cells (NPCs), which result in genomic instability and glioma formation and support the notion that metabolic stress triggers the conversion of normal NSCs to a glioma-initiating NSCs [69].