CCL2 and steatosis: The role of NLRP3 in the development of steatosis requires CASP1-mediated inflammation, which promotes triglyceride synthesis in hepatocytes by decreasing lipolytic gene peroxisome proliferator-activated receptor-α transactivation55,56, induces tumor necrosis factor-α23 and the pro-steatotic chemokine monocyte chemoattractant protein 1 in hepatocytes, and augments TLR4-dependent up-regulation of inflammatory signaling in macrophages21,45.