This suggests that the mechanisms that control p27Kip1 levels by proteolysis are not affected by ROS levels and our findings support the hypothesis that the pro-oxidant levels of melanoma cells allow the nuclear exportation and stabilization of p27Kip1 in the cytoplasm by its phosphorylation on S10 and T198 due to ROS-regulated signaling pathways, such as, PI3K/AKT pathway. Here, CDKN1B is linked to melanoma.