TNFSF11 and osteoporosis: Interestingly, RANKL is shared by various human forms of osteoporosis [16, 26] and, according to our previous results, RANKL-expressing EVs have biological functions, supporting osteoclast survival in vitro and triggering osteoclastogenesis when injected systemically in RANKL-null mice [37], indirectly suggesting that circulating RANKL-positive EVs could also represent biological tools contributing to exacerbated osteoclastogenesis in osteopenic diseases.