Given this evidence, we hypothesized that Shp1, whose overexpression produces a phenotype similar to that induced by glycerophosphoinositols treatment in A375MM melanoma cells, may be activated by glycerophosphoinositols binding also in cancer cells, thus leading to a reduction in invadopodia function (similarly to the mechanism identified in fibroblasts [16]). This evidence concerns the gene PTPN6 and melanoma.