Mice deficient in ERK5 show increased food intake and as a result, demonstrate increased adiposity.[88] Another study also reported implications behind type II DM and obesity due to ERK5 deficiency specifically in leptin receptor (LepR)-expressing neurons of female mice showing impaired glucose tolerance, food intake, energy expenditure, and decreased physical activity.[131] Furthermore, studies on regulators of the MAPKs pathway can also help to account for the molecular mechanism behind obesity. This evidence concerns the gene LEPR and Obesity.