These studies imply that SCD1 is a critical mediator of metabolic syndrome; however, unexpectedly, the absence of SCD1 either by gene deletion or antisense oligonucleotide accelerated atherosclerosis in a mouse model of hyperlipidemia and atherosclerosis on a Western diet despite relatively reduced plasma TG and increased insulin sensitivity [12], [13]. The gene discussed is SCD; the disease is metabolic syndrome.