Knock-out mice studies with TLR-4 deficiency and intestinal sterilization with non-absorbable antibiotics have found a reduction in steatosis, oxidative stress, and liver inflammation with a consequent decrease in HCC risk development[50,51], although the risk for liver injury increased, probably due to a deficiency in the innate immunity caused by the suppression of TLR-4. This evidence concerns the gene TLR4 and steatosis.