Furthermore, amplified N-Myc can directly bind with the tetrameric form of p53 at the C-terminal domain in the nucleus to alter p53-dependent transcriptional responses in neuroblastoma patients with wild-type p53, but wild-type p53 negatively regulates G6PD activity, a rate-limiting enzyme of the pentose phosphate pathway that is the most important sources of nucleotides, and then decreases dNTP synthesis, ultimately influencing the DNA repair [46, 68, 69]. This evidence concerns the gene TP53 and neuroblastoma.