Activation of RAS in the bone microenvironment has been shown to contribute to osteoporosis by stimulating the release of receptor activator for nuclear factor-κ B Ligand (RANKL) from osteoblasts (22–24), while inhibition of local RAS activation can alleviate bone loss and accelerate bone healing and remodeling (21, 25). The gene discussed is TNFSF11; the disease is osteoporosis.