It is shown that Gln deprivation leads to interactions between the expression of MYC members (MYCN and C-MYC), thereby damaging the phenotype and radiation resistance of CSCs in neuroblastoma [264].In addition, there is evidence that Gln deprivation through regulation α-Ketoglutaric acid (α-KG, a cofactor of chromatin modifying enzymes) contributes to increased H3K27 trimethylation to induce CSC gene dysregulation, indicating that Gln can affect the characteristics of CSCs through epigenetic pathways. The gene discussed is MYC; the disease is neuroblastoma.