In an obese mouse model, Lu et al. [10] found that the overexpression of periostin in the liver induced hepatic steatosis and hypertriglyceridemia via JNK pathway-involved downregulation of PPARα, which predominantly regulates the fatty acid oxidation in mitochondria and peroxisomes [15, 16], whereas genetic knockout of periostin or administration of a periostin-neutralizing antibody significantly improved these induced conditions. Here, MAPK8 is linked to hypertriglyceridemia.