Distinct WMS subtypes can also be caused by mono-allelic mutations in fibrillin-1 (FBN1, WMS2) or biallelic mutations in LTBP2 (WMS3) or ADAMTS17 (WMS4), suggesting that these four genes may act together in pathways that regulate development and homeostasis of affected tissues (Faivre et al, 2003b; Morales et al, 2009; Haji-Seyed-Javadi et al, 2012; Cecchi et al, 2013; Karoulias et al, 2020a; Evans et al, 2020). Here, LTBP2 is linked to Weill-Marchesani syndrome.