Although further in vitro and in vivo studies are required to analyze the effects of MR in mediating inflammation, these findings suggest that male offspring exposed to maternal HFD may tolerate acute psychological or endocrine stressors more efficiently than CHD offspring in adulthood, initiating protective, anti-inflammatory signalling through enhanced IκBα expression in the hippocampus, and reduced MR expression in the amygdala. The gene discussed is NFKBIA; the disease is coronary artery disorder.