Missense mutations in type I procollagens can also lead to rare forms of classical and vascular EDS, while complete or partial skipping of exon six in alpha1 type I (COL1A1) or alpha2 type I (COL1A2) is responsible for arthrochalasia EDS, a condition mainly characterized by congenital bilateral hip dislocation, severe generalized joint hypermobility with multiple dislocations/subluxations and skin hyperextensibility (De Paepe and Malfait, 2012; Malfait and De Paepe, 2014). Here, COL1A2 is linked to Ehlers-Danlos syndrome, vascular type.