In addition, a high proportion of the two oncometabolites, α-KG and succinate, was previously observed as a p53-dependent senescence response of KRAS-mutant cancer cells, leading to the modulation of α-KG-dependent dioxygenases and tumour suppression23; however, the mechanistic underpinnings and functional implications of altered G3P:DHAP, G3P:glycerol and pEtN:CDP-Etn ratios in senescence regulation are unknown. This evidence concerns the gene KRAS and cancer.