Second, such oxidative stress and inflammation can cause beta cell damage and insulin resistance, leading to the accumulation of fat in the liver, known as steatosis, which has been shown to cause damage in the mitochondria and endoplasmic reticulum through pathways involving JNK activation which then upregulate genes that are pro-apoptotic like PUMA24,27–29. This evidence concerns the gene MAPK8 and steatosis.