KRAS and neoplasm: Thus, Ying and coworkers, using a KRASG12D-inducing mouse model, have performed a transcriptome and metabolomics analysis of KRAS-induced tumors, showing that KRASG12D plays a key role in the control of tumor metabolism through stimulation of glucose uptake and channeling of glucose intermediates into hexosamine biosynthesis and the pentose phosphate pathway [93].