In that KRAS mutation and MYC amplification can drive glycolysis (Ying et al, 2012; Dang, 2013), the findings that signature A tumors are de‐enriched in these events relative to signature B tumors and enriched for glycolysis gene loci CNA amplifications support that tumor cells can meet their metabolic demands through distinct mechanisms, or combinations thereof. Here, KRAS is linked to neoplasm.