KRAS and cancer: A pooled CRISPR/Cas9 screen using an isogenic pair of HCT116 cell lines with and without K-Ras mutation showed that tumors with oncogenic K-Ras were highly dependent on mitochondrial oxidative phosphorylation, and inactivating metabolic enzymes such as NAD kinase (NADK) and ketohexokinase (KHK) led to reduced growth of cancer cells by 50% [39].