These findings suggest that adipose tissue dysfunction induced by obesity could alter the adipokine profile (i.e., the adiponectin/leptin ratio), leading to an imbalance in the Treg/Th17 ratio, increasing the Th2 response, and increasing secretion of pro-inflammatory cytokines into the lung, leading to an increased risk of developing respiratory diseases. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.