The type of variant involving the COL3A1 gene was also been suggested to correlate with the phenotype severity of vEDS; specifically, a subgroup of patients in a large European cohort bearing non-glycine missense and/or genetic variations at the C- and N-termini of type III procollagens was found to develop a later-onset and a milder phenotype with higher rates of aortic complications [114], while mutations at splice-donor sites were associated with higher mortality rates with respect to those involving the splice-acceptor sequences [115]. Here, COL3A1 is linked to Ehlers-Danlos syndrome, vascular type.