Moreover, synovial fibroblasts are an important source for RANKL-induced bone loss in arthritis [6], and we showed that PRL downregulates cytokine-induced expression of the RANKL gene in cultured synovial fibroblasts via a STAT3-dependent pathway, and that this hormone reduces osteoclastogenesis in co-cultures of synovial fibroblasts and osteoclast progenitor cells. This evidence concerns the gene PRL and arthritic joint disease.