To determine the additional cellular and molecular mechanisms associated with the increased severity of arthritic pathogenesis found in KLF2−/− mice, we induced differentiation of bone marrow-derived osteoclast precursor cells to osteoclasts harvested from the femurs of KLF2−/− and KLF2+/+ mice after the induction of arthritis. The gene discussed is KLF2; the disease is arthritic joint disease.