Data from pathways and tissue-specific expression analyses on these genes identified a role in CeD pathogenesis for Lipoma-Preferred Partner (LPP) [18,19,20], C1ORF106 (C1 Orfan 106), ARGHAP31 [21] and Protein Tyrosine Phosphatase Receptor Type K (PTPRK) genes, which play a role in actin-cytoskeleton rearrangement, cell-cell adhesion and in the Epidermal Growth factor (EGF)/EGF Receptor (EGFR) pathway activation [17,22]. This evidence concerns the gene EGFR and cranioectodermal dysplasia.