Moreover, we elucidated the potential mechanism by which gut-originated LPS may pass through the damaged intestinal barrier into the brain to activate the TLR4–mediated myeloid differentiation primary response protein 88–dependent nuclear factor-kappa B (TLR4/MyD88/NF-κB) pathway, resulting in a pro-inflammatory micro-environment, which seems to be an important contributor of autism. This evidence concerns the gene TLR4 and autism.