Zhang et al12 found that autophagy facilitated apoptosis in human lung cancer cells treated with Paris Saponin II, while Song et al13 showed that apoptosis and autophagy antagonized each other, such that apoptosis could be inhibited by autophagy, thus promoting cell survival.14 Our results showed that treatment with the autophagy inhibitor 3‐MA increased joint inflammation and articular cartilage injury in AA rats, while the autophagy activator Rapa reduced synovial fluid inflammation and articular chondrocyte apoptosis in vivo. The gene discussed is TRERF1; the disease is lung carcinoma.