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A schematic model of the contributor and potential mechanism of KAL in the occurrence and development of NAFLD. KAL is increased in HTG subjects and NAFLD patients. FFA, the consequent product of HTG, up-regulates KAL in hepatocytes. Elevated KAL induced hepatic steatosis and NASH by down-regulating ATGL and CGI-58 by LRP6/PKA/GSK3β pathway. Consequently, diminishing CGI-58 activated NF-κB/TNFα signaling pathway. Fenofibrate may benefit NAFLD by decreasing KAL
