Recently, arthritic hTNFα-transgenic mice transplanted with bone marrow cells lacking Atg7 (i.e., via LysMCre-mediated knockout of Atg7) were protected from TNFα-induced loss of proteoglycan and chondrocytes death, suggesting that autophagy might play a role in both the progression of experimentally induced RA and regulation of chondrocytes apoptosis [145]. Here, ATG7 is linked to rheumatoid arthritis.