KRAS and neoplasm: In contrast to the lack of Kras-dependence in vitro, mutant Kras was required and sufficient for sustained tumor growth in vivo (Figure 3f): murine cell lines expressing shKras displayed statistically (p < 0.001) and biologically (50–90% inhibition) significantly decreased tumor growth compared with parental cell lines expressing shC. Correspondingly, pKrasG12C overexpression accelerated tumor growth compared with overexpression of pC.