It is known that the replenishment reaction of the TCA cycle by the glutamine pathway is carried out when MPC is inhibited.9 Recent reports have suggested that D‐2HG, which is known as an oncometabolite, may be elevated in glutamine metabolites in colon cancer cells that do not have IDH mutation, further suggesting that D‐2HG is involved in EMT.10 We surmised that MPC knockdown decreased the supply of pyruvic acid to the TCA cycle and that the glutamine supply and metabolism might have been enhanced as a compensatory replenishment reaction. Here, IDH1 is linked to colonic neoplasm.