Furthermore, we detected elevated levels of ATGL protein in hepatocytes where TAOK1 was silenced, which is expected to impact on the increased lipid utilization by enhancing canonical lipolysis rate.46–48 In parallel, we found that the knockdown of TAOK1 in hepatocytes suppressed phosphorylation of ERK and JNK, which are critical signaling components stimulating proliferation, migration, and invasion of NASH-driven HCC.35 Consistently, we observed lower proliferative, migratory, and invasive capacity, as well as epithelial-mesenchymal transition in TAOK1-deficient hepatoma-derived cells. This evidence concerns the gene PNPLA2 and hepatocellular carcinoma.