Given the obesity-evoked increase in MAFG signaling, we hypothesized that Mafg loss in vivo could be metabolically favorable in DIO and conducted Mafg knockdown by performing biweekly injections of Mafg or Scr LNAs in CD- or HFD-fed C57BL/6N mice. The gene discussed is MAFG; the disease is obesity due to melanocortin 4 receptor deficiency.