This need is further emphasized by the observation that in KRAS mutant NSCLC cell lines, RNAi‐mediated knockdown of KRAS only partially inhibits in vivo tumor growth, suggesting that targeting oncogenic KRAS in combination with other effectors will most likely provide enhanced anti‐cancer efficacy compared to targeting KRAS alone (Sunaga et al, 2011). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.