FFAR2 and metabolic dysfunction-associated steatotic liver disease: For example, in non-alcoholic fatty liver disease-related hepatocellular carcinoma (NAFLD-HCC), acetate can inhibit tumor progression by activating the G protein-coupled receptor 43 (GPR43) 38; whereas in glioblastoma, acetate supports tumor growth by sustaining the metabolic demands of cell proliferation 39.