The extrinsic pathway typically involves death receptors, while the intrinsic pathway operates through the release of apoptotic proteins from mitochondria.[28] Some antiapoptotic proteins (e.g., BCL-2 family) maintain cell survival under normal circumstances, but in knee osteoarthritis, their expression may be dysregulated, rendering cells more susceptible to apoptosis.[29] During disease progression, OA chondrocytes produce matrix metalloproteinase 13 (MMP-13) capable of degrading collagen matrix, along with a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5). This evidence concerns the gene BCL2 and osteoarthritis, knee.