Potentially supportive of this nascent hypothesis are recent data showing modified expression and metabolic activity by GLUD1/2 in gliomas with IDH1 mutation, we identified an intronic variant in GLUD1 in our GBM CAML signature and this locus is shared with BC (although, in BC the locus is a non-signature variant) [32, 33]. The gene discussed is CAMLG; the disease is glioma.