GD, and other subtypes of the musculoskeletal disorders collectively known as acromelic dysplasias [16] arise from recessive mutations in several fibrillin-binding proteins i.e., LTBP3 (GD3, MIM 617809), ADAMTS10 (Weill-Marchesani syndrome (WMS1), MIM 277600), ADAMTS17 (WMS4, MIM 613195), LTBP2 (WMS2, MIM 614819), or dominant mutations in FBN1 (Acromicric dysplasia, MIM 102370; GD2, MIM 614185; WMS2, MIM 608328) [16]. Here, ADAMTS17 is linked to Weill-Marchesani syndrome.