eNOS-derived NO in T2D inhibits the production of M-CSF and RANKL and stimulates the production of OPG in both preosteoblasts and osteoblasts; these effects result in a decrease in recruitment of HSC and their differentiation to osteoclast (Wongdee and Charoenphandhu, 2011[164]; Catalfamo et al., 2013[23]). This evidence concerns the gene NOS3 and type 2 diabetes mellitus.