HIVEP3 and osteogenesis imperfecta: There remains a substantial unmet clinical need for OI treatments that reduce fracture risk in OI.11,30 We have previously reported that SHN3 acts as a cell-intrinsic negative regulator of both osteoblast bone formation activity and the ability of osteoblasts to promote an osteoanabolic vascular microenvironment in bone.14 Notably, the level of Shn3 expression was elevated in bulk skeletal transcriptional analysis but not isolated SSCs from Col1a2oim/oim mice (Figs. S5c and S6a).