Given the similarities between IBD and PD, the influence of diet and gut microbiome on DNA methylation [120–123], and that many PD risk factors can cause intestinal dysbiosis, it is conceivable that dysbiosis simultaneously increases LPS levels (through the growth of gram-negative bacteria) and responsiveness (e.g., altering TLR4 or inhibitory PPARγ levels), leading to excessive LPS-TLR4 signalling and inflammation in the gut. The gene discussed is TLR4; the disease is inflammatory bowel disease.