Another interpretation of these partly explained relationships supports a hypothesis that differing biological mechanisms such as immune dysregulation instead of viral persistence contribute to different clinical phenotypes (eg, linking immune dysregulation to a musculoskeletal phenotype).7 In particular, pathways involving monocyte and macrophage activation have become a focus in treated HIV infection in the past 5 years, a condition in which this immune activation is associated with atherosclerotic inflammation and for which IL-1β targeted therapies have been proposed.17,29,30. The gene discussed is IL1B; the disease is HIV infectious disease.