With a larger cohort, it can be investigated if mutant IDH1 expression results in a more metabolically homogenous tumour given the strength of this oncogenic lesion in driving tumourigenesis and metabolic reprogramming, in contrast to IDH1 wildtype GBMs that are characterised by several oncogenic lesions, including chromosome7 loss/chromosome 10 gain, CDKN2A deletion, and amplification of EGFR and PDGFRA [40]. The gene discussed is CDKN2A; the disease is neoplasm.