As corticoids are well known to depress the inflammatory response [38] and to induce lipodystrophy through the decreased expression of lipoprotein lipase, an enzyme secreted by adipocytes and involved in triglyceride synthesis [39], we hypothesize that the defective immune response and the lipodystrophy induced under corticotherapy may favor the release of pathogens from AT and, consequently, the reactivation of infection. Here, LPL is linked to infection.