Targeted deletion of BK channel in mice resulted in an osteoclast-autonomous osteopenia, being apparent in juvenile females displaying normal bone-influencing endocrinology and osteoclastogenesis, accompanied by increased plasma Cathepsin K levels, reduced bone mineral density and enhanced porosity of trabecular micro-architecture, but without obvious fragility fractures. The gene discussed is KCNMA1; the disease is Osteopenia.