To further investigate whether p16INK4a wasunique in promoting SAHF formation we developed a transient melanoma model torapidly assess the functions of the p21Waf1 and p16INK4a.The functionally impaired p16INK4a_R24P mutant that is unable to bind and inhibit CDK4 butretains CDK6 inhibitory activity was used as a control [34,39].The WMM1175 melanoma cells were transiently transfected with plasmids encoding each ofthese CDK inhibitors along with a plasmid encoding the enhanced greenfluorescent protein (EGFP), which was used as a marker of transfection. The gene discussed is CDK6; the disease is melanoma.