Tenta et al. identified a role in the induction of osteoclastogenesis by the nuclear factor-kappaB activating receptor (RANKL) and the RANK decoy osteoprotegerin (OPG) receptor, revealing a significant overregulation of the OPG/RANKL ratio in SGA infants, highlighting their role in bone turnover in compensating for intrauterine growth retardation [10]. Here, TNFSF11 is linked to fetal growth restriction.