Additionally, changes in various inflammatory cytokines, such as TNF-α and IL-1β, may further indirectly promote neurotoxicity through a variety of mechanisms, including Ca2+ overload [484], alterations in dendritic spine length [153, 154], and axonal degeneration [479], all of which are associated with cognitive deficits, particularly in the cART era [104–106]. The gene discussed is IL1B; the disease is Cognitive impairment.