To date, it is known that CB1R activation aggravates inflammation, steatosis, and fibrosis through the reduction of fatty acid oxidation and TG-VLDL secretion, enhanced de novo lipogenesis, and activation of HSCs, whereas CB2R inhibits inflammation and steatosis and has anti-fibrotic properties by exerting anti-inflammatory functions on Kupffer cells.29,32, Figure 3 summarizes the opposite roles of CB1R and CB2R in the progression of ALD. Here, CNR1 is linked to steatosis.