In particular, B cells [148–150] and B-cell-derived plasma cells in multiple myeloma (MM) have been reported to have the potential to support osteoclastogenesis [151], possibly via direct expression of RANKL [152], decoy receptor 3 (DcR3) [153], or as an indirect consequence of IL-7 secretion [154, 155], a potent stimulator of bone resorption in vivo [156]. Here, TNFRSF6B is linked to AL amyloidosis.