Human EDS forms are grouped based on the underlying pathogenetic mechanisms related to primary structure and processing of collagen (COL1A1, COL1A2, COL3A1, COL5A1, COL5A2, ADAMTS2), collagen folding and cross-linking (PLOD1, FKBP14), structure and function of the myomatrix (TNXB, COL12A1), glycosaminoglycan biosynthesis (B4GALT7, B3GALT6, CHST14, DSE), complement pathway (C1S, C1R), and intracellular processes (SLC39A13, ZNF469, PRDM5) [3]. This evidence concerns the gene COL5A2 and Ehlers-Danlos syndrome.