Oxidative stress and lipolysis due to obesity-associated inflammation, which is indicated by elevated levels of TBARS, NEFA, and SAA in basal and postoperative LDL (Fig. 1A–C), as well as increased plasma CRP one year postoperatively (7), contribute to these proatherogenic LDL alterations. The gene discussed is CRP; the disease is obesity due to melanocortin 4 receptor deficiency.