KRAS and cancer: In general, metabolic reprogramming can be orchestrated by cancer genes such as K-RAS, c-MYC, PI3K, TP53, AMPK and their signalling, which enhance the glycolytic and glutamine pathways to support biosynthesis, redox homoeostasis, cell growth, survival and enhanced drug resistance.10–13 Furthermore, other global modulators of cell biofunctions such as mTOR and HIF-1α, may accentuate these effects by acting pleiotropically to modify the overall cell metabolism, biosynthetic pathways and drug response.14,15