Finally, loss-of-function mutations in Golgin GMAP-210 (TRIP11) causes a lethal skeletal dysplasia in both mice and humans (achondrogenesis type 1A) [39], which is characterized by disrupted Golgi architecture and ER stress due to the intracellular accumulation of perlecan (but not aggrecan or type II collagen) eventually leading to abnormal chondrocyte differentiation and increased apoptosis (Table 2) [39]. This evidence concerns the gene TRIP11 and skeletal dysplasia.