They found the combined disruption of 4e-bp1 and 4e-bp2 in mice increased their sensitivity to diet-induced obesity by accelerated adipogenesis driven by increased expression of C/ebpδ, C/ebpα, and Pparγ coupled with reduced energy expenditure, reduced lipolysis and greater fatty acid reesterification in the adipose tissue of 4e-bp1 and 4e-bp2 double KO mice [65]. Here, PPARG is linked to obesity due to melanocortin 4 receptor deficiency.