IDH mutations impede cellular metabolism and hinder tumor growth in three main ways: (1) under hypoxic conditions, mutant IDH1 cannot undergo reductive carboxylation, (2) the chemical reaction induced by mutant IDH consumes NADPH, so tumors are more susceptible to free radical damage, (3) D-2-hydroxyglutarate directly inhibits ATP synthase by binding to it and affects ATP production under limiting glucose conditions [37]. Here, IDH1 is linked to neoplasm.