Together, although the individual effects of exogenously supplemented molecules on restoring growth were generally mild, the results suggest that mainly the decreased CDK2 and OPN levels may be partly responsible for the proliferation defect and a combined decrease of survival factors might contribute to growth inhibition and apoptosis, either directly or indirectly, elicited by blocking the SWI/SNF function in melanoma cells. This evidence concerns the gene CDK2 and melanoma.