In the past year, complex interactions between Ras and the cell cycle have been identified. In primary cells, activated Ras induces a cell-cycle arrest via the induction of cyclin-dependent kinase inhibitors (CDKIs). Oncogenic changes that cooperate with Ras act by neutralising CDKIs by various mechanisms. In the absence of a negative growth signal from Ras, such as in most immortalised cell lines, Ras acts positively on the cell cycle. Insights have been made into the mechanisms by which Ras abrogates remaining cell-cycle controls.