Since all reported cases of ACG1A to date are due to mutations in TRIP11 (17, 18), which encodes a golgin also known as GMAP-210 (Golgi-microtubule-associated protein, 210 kDa), we were curious to find out whether the striking clinical similarity of LBR- and TRIP11-associated achondrogenesis point to a common Golgi-related pathophysiology. Here, LBR is linked to achondrogenesis type IA.