These obesity-associated changes adversely influence essential aspects of LDL functionality: 1) they diminish nonatherogenic binding to LDLR (Fig. 2D); 2) they enhance proatherogenic binding to CD36 and LOX-1 receptors (Fig. 2E, F); 3) they enhance proatherogenic binding and retention by extracellular matrix components (Fig. 4). The gene discussed is CD36; the disease is obesity due to melanocortin 4 receptor deficiency.