The canonical Wnt signalling pathway, which has an important role in bone formation, is negatively regulated by Axin1 and its homologue Axin2 through their capacity to degrade β-catenin. Previous work has shown that Axin1 and Axin2 have distinct but overlapping functions: deletion of Axin1 is embryonic lethal in mice, whereas deletion of Axin2 has less marked effects. On page 3566, Di Chen and colleagues investigate the unique role of Axin2 in bone remodelling in a study of Axin2-deficient mice. Their analyses show that, compared with wild-type mice, Axin2-deficient adult mice have greater bone mass and a higher rate of bone formation. The authors show that this is due to an increase in the proliferation and differentiation of osteoblasts (which build bone) as well as a decrease in the formation and function of osteoclasts (which resorb bone). Because most of the alterations in Axin2-deficient cells are rescued in the absence of β-catenin expression, the authors conclude that β-catenin activation underlies the increase in osteoblast function and bone formation observed in Axin2-deficient mice. Finally, the authors provide additional evidence that bone remodelling involves crosstalk between Axin2–β-catenin signalling and the bone-morphogenetic-protein pathway. These data increase our understanding of bone remodelling at the molecular level, which is relevant for managing and treating osteoporosis.