IL12A and neoplasm: D‐2‐HG can lead to specifically educated, dysfunctional DCs by reprogramming of the lipopolysaccharide (LPS)‐induced metabolism,38, 40 promoting oxidative phosphorylation, inhibiting glycolysis, and inhibiting p34/IL‐12A and p35/IL‐12B expression,41 thus reducing IL‐12 and promoting immune escape from tumor cells.42