Importantly, fat transplant experiments showed that adipose-specific JNK inactivation in the visceral fat was sufficient to protect mice with apolipoprotein E (ApoE) deficiency from atherosclerosis, with the beneficial effects attenuated by the continuous infusion of recombinant AFABP, supporting the participation of adipocyte-derived AFABP as a link between visceral fat inflammation and atherosclerosis (56). The gene discussed is APOE; the disease is atherosclerosis.