Upon being translocated to metabolic tissues, LPS can elicit pro-inflammatory responses via pathways mediated primarily by TLR-4 (31) with the involvement of TLR-2 (32) and TLR-9 (33), diminishing insulin signaling and increasing adiposity in the state of obesity and T2DM. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.