Since mutations in TP53 gene are present in the majority of DIPG cases, and given the increased tumor aggressiveness and worse overall prognosis associated with TP53 mutations DIPG, we investigated the efficacy of mutant p53 targeting with APR-246, a molecular agent shown to form covalent bonds with mutant p53 protein and to induce oxidative stress by glutathione depletion and thioredoxin reductase inactivation in a variety of cancer types [14,18]. This evidence concerns the gene PRDX5 and neoplasm.