In addition to leptin promoting profibrogenic responses via TGF-β signaling [83,84], obesity-induced leptin exacerbates NASH via enhancing the responsiveness to endotoxins [85], suggesting that leptin plays a key role in proinflammatory, profibrogenic processes involved in the progression of NAFLD. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.