Other oncogenic mechanisms specific of the R-2HG concern the selective inhibition of the α-KG-dependent branch chain amino acid transaminases 1 (BCAT1) and BCAT2 [178], decreasing glutamate levels and making cells auxotrophic for this amino acid as well as for glutamine necessary to continuously replenish the NADPH consumed by mutant IDH and essential to fuel the cellular anabolism that supports the tumour growth [179]. The gene discussed is IDH1; the disease is neoplasm.