To be consistent with the preclinical (25) and human data we generated, only adults (n = 8) with clinically moderate-to-severe OI caused by glycine substitution mutations in COL1A1 or COL1A2 or biallelic pathogenic variants in CRTAP, PPIB, or LEPRE1, i.e., structural mutations affecting type I collagen or mutations affecting the posttranslational modification machinery of type I collagen, were enrolled (Table 2). The gene discussed is P3H1; the disease is osteogenesis imperfecta.