In this regard, Cohen-Kfir and colleagues (2011) observed a significant reduction in bone mass and upregulated adipogenesis in the bone marrow of SIRT1 haplo-insufficient (SIRT1+/−) female mice, suggesting a crosstalk between metabolic organs and bone and proposing SIRT1 as a potential therapeutic target for the prevention of metabolic diseases and the development of osteoporosis [26,27]. The gene discussed is SIRT1; the disease is Other metabolic disease.