However, scholars have conflicting views on the targets and pathways of PPARγ in osteoarthritis, with some studies demonstrating that PPARγ can maintain chondrocyte viability by the Akt/mTOR pathway to induce chondrocyte autophagy [31], and others finding that PPARγ can inhibit chondrocyte apoptosis and reduce the inflammatory response by inhibiting MAPK and NF-κB activation [32]. Here, NFKB1 is linked to osteoarthritis.