That is to say, during melanoma progression, the loss of E-cadherin expression [6] disrupts normal homeostasis by freeing melanoma cells from structural and functional regulation by keratinocytes and is paralleled by a gain in N-cadherin function [4] that mediates homotypic interaction between melanoma cells, facilitates gap-junctional formation with fibroblasts and endothelial cells, and promotes melanoma cell migration and survival [7]. This evidence concerns the gene CDH2 and melanoma.