A possible mechanism involves the PI3K-Akt pathway as it has been shown both that CD146 activates the PI3K-AKT pathway in melanoma cells and that reduced expression of JAM-A increases the pool of available PIP3 [31], [32]; one could hypothesize that JAM-A blocked the pro-migratory function of CD146 by trapping PIP3 and that high expression of JAM-A in MCF-7 cells prevents part of CD146 signaling via PI3K-Akt. This evidence concerns the gene AKT1 and melanoma.