Given the reduced growth rate in Suit-2 after K-Ras depletion, it is reasonable to assume that it is K-Ras-driven G2 cyclin production that supports the maintenance of cancer cell division; however, this is not linked to any inhibition of exit from G2 (as would be expected if cyclin levels were maintained at a high level), given that the relative level of exit from G2 compared to exit from G1 is actually decreased through the knockdown of mutant K-Ras (Figure 3). This evidence concerns the gene KRAS and cancer.