TNFα promotes bone resorption in RA, as it is able to increase osteoclast recruitment, differentiation, and activity both directly, in the presence of minimal concentration of RANKL or even in the absence of RANKL signalling [15, 16] and indirectly by increasing the expression of osteoclast activators (M-CSF and RANKL) in several cells such as osteoblasts and cells of immune system [17–19]. Here, TNF is linked to rheumatoid arthritis.