To further explore the protective effect of PRL against inflammation and osteoclastogenesis in arthritis, mice null (Prlr-/-) or not (Prlr+/+) for the PRL receptor were subjected to MAIA, as this is a highly efficient model for inducing unilateral joint inflammation and bone erosion in the genetic background (C57BL6) of these mice [23]. This evidence concerns the gene PRLR and arthritic joint disease.