Moreover, the imbalance between Th17 and T-regulatory lymphocytes influences inflammation and osteoclastogenesis in arthritis [30], and PRL blocked the AIA-induced increase in the joint expression of the genes Rorc and Rora encoding for retinoic acid orphan nuclear receptors RORγt and RORα, respectively, which are transcription factors specific for Th17 cells, and the expression of the Th17 cell cytokine genes, Il17a, Il21, and Il22 (Fig. 1g). The gene discussed is PRL; the disease is arthritic joint disease.