The association between fat redistribution, glucose disturbances, IR and cART, might be explained through several mechanisms: lipoatrophy per se; lipotoxicity (cART or visceral fat-induced or both, demonstrated by increased lipolysis and circulating free fatty acids) [2]; inflammation (resulting from the infection and demonstrated by increased TNF-alpha production, increased serum concentrations of the soluble type 2 receptor of TNF-alpha [39] and other interleukins), and hormonal factors (leptin, resistin or adiponectin). The gene discussed is RETN; the disease is infection.