Based on the in vivo mouse experiments confirming that silencing of RUNX2 leads to increased bone turnover rate, decreased bone density, and bone strength in CKD-MBD mice, as well as the partial results of the in vitro experiments showing that CK2 phosphorylates and activates RUNX2, recruiting USP7 to stabilize RUNX2 expression and promote the differentiation of osteogenic precursor cells into mature osteoblasts, we postulated that CK2 could improve MBD in CKD-MBD mice through regulating RUNX2 expression. Here, RUNX2 is linked to chronic kidney disease.