Some studies have documented that the chloride channel acts as the Cl−/H+ exchanger, which is regulated by a voltage-gating mechanism, and plays a very important role in the acidification of osteoclast-mediated degradation of bone tissue; mutations in CLCN7 may be responsible for various types of osteopetrosis [27, 28]. Here, CLCN7 is linked to osteopetrosis.