ATG16L1 and hepatocellular carcinoma: For example, Du et al. found that significantly upregulated circMDK in HCC is associated with m6A modification and poor survival in HCC patients, and it can enhance the expression of ATG16L1 by binding to miR-346 and miR-874-3, thereby activating the PI3K/AKT/mTOR signaling pathway and promoting the progression of HCC.