Consistently, we have demonstrated that the reduced BQI-SDS in 4 out of 5 patients is also inversely related to sRANKL and CTX I. It is important to remember that one of the major sources of RANKL and OPG is osteoblasts, and we have previously reported that the sera of OI patients in vitro can inhibit osteoblast differentiation as well as reduce OPG secretion without altering RANKL production [22], thus, supporting our findings in the present paper. This evidence concerns the gene TNFSF11 and osteogenesis imperfecta.