Under hypoxic conditions, mammalian cells produce L‐2‐HG that is sufficient to induce a characteristic hypermethylation phenotype of histones similar to that observed in IDHmut contexts.[31] L‐2‐HG promotes HIF‐1α stabilization and sustains tumor growth, while the role of D‐2‐HG on HIF‐1α stability is diverse in a context‐dependent manner.[32, 33] In glioma, understanding whether and how IDHmut affects the level of HIF‐1α is important to comprehend how oncogenic IDH mutations promote tumor adaptation to oxygen and nutrition limitation. The gene discussed is HIF1A; the disease is glioma.