To directly investigate the contribution of genetic mutations/copy number aberrations to metabolic phenotype, we asked whether metabolite or transcript levels were differentially expressed in the presence/absence of the four most common somatic genotypes described in previous genomic analysis of HCC: mtDNA mutations, gLOH, telomerase reverse transcriptase (TERT) mutations, and mTOR pathway alterations (Table 1). This evidence concerns the gene MTOR and hepatocellular carcinoma.