Bone resorption is regulated by the immune system, where receptor activator of nuclear factor (NF)κB ligand (RANKL), a new member of the tumor‐necrosis factor family, may contribute to pathological conditions. Due to the role of RANKL in the maturation of monocyte‐derived osteoclasts, we hypothesized that RANKL could exert chemotactic properties toward monocytic cells. Our results demonstrate that RANKL induces the migration of MonoMac‐6 monocytic cells as well as human freshly isolated total peripheral blood mononuclear cells (PBMC) and CD14⁺ purified PBMC. RANKL induces the migration of MonoMac‐6 cells in a dose‐dependent manner and with an efficacy similar to MCP‐1. After an 8‐h incubation, the soluble form of RANKL (sRANKL) started to exhibit a chemoattractive effect on MonoMac‐6 cells, with an increased effect observed up to 24 h. RANKL elicits an additive chemotactic effect to MCP‐1. Furthermore, addition of the RANKL decoy receptor osteoprotegerin in the lower well or RANKL in the upper well abrogates the RANKL‐induced migration of MonoMac‐6 cells, hallmarking a true specific activity. RNase protection assay experiments indicate that exposure of MonoMac‐6 cells to RANKL had no significant effect on the expression of a variety of chemokines, known to attract monocytes. This study provides evidence that RANKL behaves as a chemotactic factor for monocytic cells, emphazing the cross‐talk between bone and immune systems.