Inflammation disrupts Smad2/3 signaling in chondrocytes through linker region (de)phosphorylation, offering a novel therapeutic target.518 Additionally, the TGF–β/TAK1–FoxO1 axis regulates articular cartilage autophagy and homeostasis, presenting a therapeutic target for OA-like joint disorders,519 while the local delivery of Cbfβ preserves TGF-β signaling in cartilage and may prevent OA progression.520 ECM biosynthesis-guided scaffolds loaded with TGF-β promote neocartilage regeneration,521 highlighting a translational strategy for structural cartilage repair. Here, TGFB1 is linked to arthropathy.