Cell anchorage to the extracellular matrix (ECM) controls the cell proliferation in all multicellular organisms and the abrogation of this control is an indicator of cellular transformation. In fact, two distinct periods of the cell cycle are subject to anchorage-dependent regulation. Firstly, anchorage exerts an extensive control of the G(1)-phase, a control that we found to be more rigorous than for example the control by growth factors. Secondly, anchorage regulates the progression through cytokinesis. In order to achieve anchorage-independent growth a cell must circumvent these controls. To this end, we recently found that oncogenic H-RasV12 can provide sufficient signals to overcome the anchorage-dependence for cytokinesis. Together with earlier findings on G(1)-phase control, this demonstrates that oncogenic signaling contributes to de-regulation of anchorage-dependence during both the G(1)-phase and the cytokinesis. This also suggests that de-regulated cytokinesis may be part of oncogenic transformation.