RELA and arthritic joint disease: However, these defects were partially rescued when the RelB gene was knocked down in p100−/− mice.190 Using tissue-specific knockout mice, Kobayashi, H. et al. found that Rela/p65 deletion in embryonic limb cartilage promoted apoptosis of chondrocytes leading to impaired skeletal growth, while homozygous knockout of Rela in articular cartilage at seven weeks resulted in accelerated progression of arthritis, but heterozygotes knockout led to delayed OA development by inhibiting the expression of catabolic genes.191