Thus, the lack of oncogenic effects by forced expression of WT-DLC1 or K714E-DLC1 in high DLC1-expressing A375 and WM266-4 cells could be due to limited availability of cofactors that might be required for translocating exogenous DLC1 into the nucleus, implying that DLC1 may function with cofactors in the nucleus to promote melanoma growth and invasion in a RhoGAP-independent manner. The gene discussed is ARHGAP1; the disease is melanoma.