The most important osteoclast differentiation regulator is receptor activator of nuclear factor kappa-B ligand (RANKL), which is also mediated by cAMP.[35] However, in contrast to Cbfa1, the expression of RANKL was significantly enhanced by angiotensin II.[36] In addition, high blood pressure related risk factors are also conducive to promoting the expression of RANKL and osteoclast activity.[37–41] It was hypothesized from our team that angiotensin II changed the expression ratio of Cbfa1/RANKL through the cAMP signaling pathway, which ultimately lead to an imbalance of bone turnover. This evidence concerns the gene AGT and hypertensive disorder.