One study demonstrated increased toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway activity in diabetic vs. non-diabetic rats, with higher TLR4 expression on hepatic macrophages (FC = 2.25, p < 0.05), contributing to steatosis, inflammation, hepatocyte ballooning and fibrosis in diabetes liver [28]. This evidence concerns the gene TLR4 and steatosis.