For instance, circMDK has been shown to promote HCC tumorigenesis and progression by upregulating ATG16L1 expression through the sequestration of miR-346 and miR-874-3p [9], whereas circGPR137B inhibits HCC growth and metastasis via the circGPR137B/miR-4739/FTO feedback loop, presenting a potential therapeutic target in HCC treatment [10]. The gene discussed is ATG16L1; the disease is hepatocellular carcinoma.