Interestingly, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), which increase under pathological conditions, such as rheumatoid arthritis (RA) and osteoporosis, induce the expression of RANKL in osteoblasts and stromal cells, eventually enhancing osteoclast formation (5, 6). This evidence concerns the gene TNFSF11 and rheumatoid arthritis.