Several lines of evidence pointed out that metabolic syndrome is a frequent manifestation in SLE patients, with approximately 35% being overweight and another 27% obese.1 Obesity is, per se, a proinflammatory status in which there is an increased gene and protein expression of proinflammatory molecules such as IL-17, IL-23 and TNF-α.2 In childhood-onset SLE, TNF-α levels are associated with obesity and body fat content. The gene discussed is TNF; the disease is obesity due to melanocortin 4 receptor deficiency.