Taking into account the role played by EP4 in the differentiation of Th1 lymphocytes and in the expansion of Th17 cells [7, 8] (both implicated in RA pathogenesis [32]), and that the lack of Ptger4 or its blockage ameliorates the disease in several mouse arthritis models (collagen-induced [5, 8], collagen antibody–induced [10], and glucose-6-phosphate isomerase–induced arthritis models [8]), we decided to analyze the role of PTGER4 in RA severity. This evidence concerns the gene GPI and arthritic joint disease.