It has also been found that CHE can promote apoptosis and autophagy in rheumatoid arthritis by influencing the expression of genes related to autophagy and apoptosis (including Bax, Bcl-2, PARP, and ULK1) and the AMPK/mTOR/ULK-1 signaling pathway, thus inhibiting rheumatoid arthritis in vivo and in vitro (Cai et al., 2022). This evidence concerns the gene MTOR and rheumatoid arthritis.