Other studies also confirmed the implication of CB1R in the pathogenesis of NAFLD, as the activation of hepatic CB1R triggered lipogenesis pathways in the liver, as well as monounsaturated fatty acid accumulation and the inhibition of FAAH, which was followed by an increased level of AEA, resulting in the setting of steatosis and insulin resistance, which are the main causes of NAFLD [49,55,56,57,58]. This evidence concerns the gene CNR1 and Insulin resistance.