Intriguingly, T3 excess and E2 deficiency also share commonalities in regulating bone formation by stimulating NO cGKii pathway activity.(24) Notwithstanding the reported positive impact of CNP on osteoblastogenesis in vitro(4, 25) and in vivo,(26) with respect to CNP actions in bone, our findings suggest that actions modulating resorption predominate, at least in settings of increased bone turnover in women associated with hyperthyroidism or estrogen deficiency. This evidence concerns the gene PRKG2 and hyperthyroidism.