When these receptorsare activated, myeloid differentiation primary response protein 88(MyD88, adaptor proteins of Toll-like receptors) is recruited andpro-inflammatory signaling cascades are activated, for example, theaforementioned NF-κB pathway.84 Moreover,deletion of MyD88 has been shown to protect against obesity and insulinresistance in mice.85 The gene discussed is MYD88; the disease is obesity due to melanocortin 4 receptor deficiency.