With the advent of combined antiretroviral treatment, the nature of HIV disease has largely shifted from one of immunodeficiency to one of chronic and persistent inflammation and it is recognized that both phenomena are tightly linked in both untreated and treated disease.1 In the current study, we conclude that gp120 interferes with the cholinergic anti-inflammatory response because we found that α7 activation is no longer able to reduce the production of proinflammatory ILs and some chemokines (Figures 6 and 8). The gene discussed is ITIH4; the disease is immunodeficiency disease.