However, in AD, there is evidence that IL-1β synthesis remains unabated [19], indicating that IL-β-induced APP and P-tau production is continuing, favoring—as noted in AD pathology—accumulation of Aβ aggregates in extraneuronal plaques and intraneuronal neurofibrillary tangles, which are ubiquitinated and—although present in autophagosomes—remain undigested [20]. This evidence concerns the gene IL1B and Alzheimer disease.