Unfortunately, as is apparent in the aggregate-laden neuropathological manifestations of AD, any felicitous promise of IL-1β toward increasing parkin-mediated ubiquitination and subsequent lysosomal or proteasomal degradation afforded by IL-1β increase is apparently insufficient to overcome the concurrent propensity of IL-1β to promote production of the pathognomonic seed proteins of aggregates in AD and Parkinson’s [10]. This evidence concerns the gene IL1B and Alzheimer disease.