Recent data indicated that pharmacological activation of PPARα improves the metabolic milieu, hepatocyte ballooning and steatosis, and controls NFκB and JNK activation, neutrophil and F4/80 macrophage recruitment in diabetes-related NASH, but persistent liver inflammation with high serum MCP1 due to unsuppressed inflammation could limit PPARα agonist efficacy as a therapy for NASH [33]. This evidence concerns the gene CCL2 and steatosis.