In addition, the findings that RANKL and M-CSF treatment led to an increase in TRAP-positive osteoclasts and that circZNF367 contributes to bone loss, compromised trabecular microstructure and increased osteoclasts indicate the implication of circZNF367 in the activation and differentiation of osteoclasts, which are associated with bone resorption, and that modulating circZNF367 expression or activity might potentially help reducing bone loss and the risk of fractures associated with osteoporosis [6]. This evidence concerns the gene CSF1 and osteoporosis.