Because previous studies have reported intracellular SIRT2 plays a role as a tumor suppressor due to its impact on genomic stability, we used the CRISPR/Cas9 lentivirus and Flag-tagged transfection systems to manipulate SIRT2 expression in B16-F10 melanoma cells to determine whether intracellular SIRT2 status is responsible for the observed tumor growth. The gene discussed is SIRT2; the disease is neoplasm.