KRAS and neoplasm: Ablation of oncogenic KRAS in a mouse model of pancreatic cancer markedly reduced tumor size and also revealed a subpopulation of surviving tumor cells which did not express KRAS. These surviving cells relied heavily on oxidative phosphorylation and were sensitive to oligomycin treatment, providing evidence that inhibition of mitochondrial function may effectively target cells that survive after suppression of oncogenic KRAS signaling [59].