Martin et al. (2008) reported that FABP1-ablated mice exhibited increased age-dependent obesity, which is in line with our study. Taken together, increased lipogenesis and decreased fatty acid uptake, but not fatty acid oxidation or lipid export pathways, account for excess triglyceride accumulation in the liver in response to PM2.5 exposure. The gene discussed is FABP1; the disease is obesity due to melanocortin 4 receptor deficiency.