It is surmised that a fine balance or spatiotemporal control mechanisms exist to ensure availability of PTHrP for enhancing osteoblast differentiation, as persistently increased local PTHrP levels would favor increased osteoclast formation, through stimulation of RANKL production resulting in increased bone resorption, and high-turnover osteoporosis [19]. Here, TNFSF11 is linked to osteoporosis.