huTNFtg;TgCol6a1-Mir221/222;Mir221/222-/- mice exhibited synovial hyperplasia, cartilage destruction, and number of osteoclasts as the huTNFtg;TgCol6a1-Mir221/222;Mir221/222 d/f, f/- mice (Figure 2G), indicating that SF-specific Mir221/222 overexpression even in the absence of Mir221/222 in other cell types is sufficient to deteriorate arthritis manifestations. Here, MIR221 is linked to arthritic joint disease.