The current strategies for targeting macrophages to treat fatty liver disease mainly include the inhibition of macrophage activation (e. g., via inhibiting the inflammasome assembly), regulation of macrophage polarization (e. g., via promoting polarization into the M2 phenotype through nanoparticles), inhibition of monocyte recruitment and infiltration (e. g., via suppressing the expression of chemokines like CCL2, CCL10, or CCL3), and amelioration of toxic lipid accumulation (e. g., via promoting lipolysis, FFA efflux, and transformation to nontoxic TG) (184–186). Here, CCL3 is linked to fatty liver disease.