Co-dependence on EGFR and mutant K-Ras may reflect the fact that they can activate the cell cycle via cyclin D expression independently [29], and this is supported further by the observation that the inhibition of various forms of cyclin-dependent kinase (including CDK1 and 2) is equivalent in action to the inhibition of mutant K-Ras in cancers that are addicted to K-Ras [30]. The gene discussed is EGFR; the disease is cancer.