For example, postmenopausal osteoporosis is increasingly acknowledged as an inflammatory disease and was (re)named immunoporosis (27–30), where activated T-cells establish chronically increased bone resorption by stimulating osteoclast differentiation through RANKL-dependent and RANKL-independent pathways (31, 32). The gene discussed is TNFSF11; the disease is postmenopausal osteoporosis.