An excess of CCN2 in the bone microenvironment is also detrimental as its constitutive overexpression in osteoblasts results in their decreased differentiation,[13] as well as osteopenia in a transgenic mouse model.[14, 15] One potential mechanism is a negative regulatory role with bone morphogenetic protein (BMP)‐2.[13] In addition to its role in osteoblasts, CCN2 is also necessary for osteoclast formation and function. The gene discussed is CCN2; the disease is Osteopenia.