In MYC-driven cancers, more glutamine flow helps α-KG-dependent histone demethylation at oncogenic sites, hence encouraging tumor development119,120 On the other hand, in situations of nutrient deprivation or therapeutic resistance, a drop in α-KG level can block demethylase activity, causing the accumulation of repressive histone modifications like H3K9me3 and H3K27me3, which supports a more stem-like or quiescent state favorable for tumor survival121,122. The gene discussed is MYC; the disease is neoplasm.