With regards to the role of lipases, loss-of-function studies on hepatic lipase and LPL in the liver showed that knockout of hepatic lipase resulted in increased hepatic steatosis and inflammation in mice fed a high-fat high-cholesterol diet that might be due to the activation of stress pathways like SAPK/JNK and p38 [26]. The gene discussed is LIPC; the disease is Hepatic steatosis.