C-reactive protein promotes the inflammatory response of atrial fibrillation through the overexpression of TGF-β related to the TLR-4/NF-κB/TGF-β signaling pathway in HL-1 cells [34], while IFN-γ was reported to contribute to the hepatic inflammation in HFD-induced nonalcoholic steatohepatitis by STAT1β/TLR-2 signaling pathway in mice [35]. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatohepatitis.