NFKB1 and Brain atrophy: Brain infarcts found in IP patients[30-32] supported the hypothesis of vascular pathogenesis of CNS lesions in IP, whereas findings of brain atrophy[11,20], corpus callosum lesions[14,20], disorder of myelination[27,33] and lack of relationship between brain abnormalities and vascular patterns[14,26] supported the hypothesis of disorder of the NF-κB metabolic pathway in neurons and glia cells as a pathogenetic mechanism.