Together, these evidence and our results suggest the hypothesis that NF-κB pathway dysregulation could play a significant role in RTT pathophysiology, as already proven in rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, atherosclerosis, systemic lupus erythematosus, type I diabetes, chronic obstructive pulmonary disease and asthma [54]. This evidence concerns the gene NFKB1 and multiple sclerosis.