We find that in addition to the significant decrease in ADAM11 (Figures 9, 10), there was also a significant increase in CYCLIND1. While there is no causal relation in this observation, our data from Xenopus embryos and mouse B-16 melanoma cells shows that decreasing Adam11 protein level is sufficient to increase β-catenin activity and CyclinD1 expression, suggesting a conserved function of Adam11 in cancer. This evidence concerns the gene ADAM11 and melanoma.