Increased osteoclastogenesis in arthritic mice with or without CS exposure was blocked by local knockdown of miR-132 in joints.188 Unfortunately, despite the high miR-132 expression induced by AHR activation in RA Th17 cells, the authors failed to reveal an intrinsic role of miR-132 in Th17 cell differentiation. The gene discussed is AHR; the disease is rheumatoid arthritis.