In this sense, TIGAR, a p53 target gene often overexpressed in glioblastoma, protects glioma cells under hypoxic conditions against oxidative stress death, inhibiting the glycolytic pathway by reducing F2,6BP levels and diverting Glu uptake to PPP in the presence of TKTL1, increasing NADPH and GSH synthesis [163] (Figure 4). This evidence concerns the gene TKTL1 and central nervous system cancer.