In the current study, we have focused on the contribution of the DLC1 START domain (DLC1-START) to the full activity of DLC1, based on the hypothesis that the interaction of DLC1 with additional macromolecules through regions other than its RhoGAP domain may reveal new DLC1 scaffolding functions that could regulate its tumor suppressor activity, likely in a RhoGAP independent manner. The gene discussed is ARHGAP1; the disease is neoplasm.