This presentation reports on an ongoing study designed to test the effects of KT109 and a supplemental, proprietary drug in reducing inflammation in those suffering from non-alcoholic fatty liver disease (NAFLD). NAFLD involves the excess of fatty tissue in the liver and can lead to non-alcoholic steatohepatitis (NASH) and cirrhosis. Certain endocannabinoids, which are upregulated by steatogenic agents found in high fat diets, are involved in regulating inflammation. This study explored possible mechanisms for reducing inflammation via increasing the efficacy of our liposomes in inhibiting macrophage signaling. Diacylglycerol lipase-beta (DAGLβ) is an enzyme that produces numerous endocannabinoids involved in inflammatory signaling. KT109 is a compound known to inhibit DAGLβ, therefore inhibiting the production of inflammation inducing endocannabinoids. Liposomes are lipid vesicles that can be used to increase the efficiency of delivering drugs and reduce toxicity. Previously, we have tested the ability of using macrophages to localize the delivery of KT109 to cells, using liposomal KT109. A single dose of the liposome solution was injected into mice, and after 4 hours their organs were harvested and tested. We found that liposomal KT109 increases efficiency of inhibiting macrophage inflammation signaling, finding that 5 micrograms of the liposomal KT109 can inactivate around 80% of DAGLβ in macrophages. It was also found that the liposomes had the greatest effect in the liver, giving it a high potential to be effective in treating NAFLD and NASH. Our study proposes a novel treatment of NAFLD and NASH via liposomal forms of KT109 with a supplemental drug.