The study found that knockdown of Acc significantly elevated plasma TG levels (200%) (Kim et al., 2017), and that Acc knockdown decreases the concentration of PUFA and thereby increases SREBP-1 activity, whereas restored-activated SREBP-1 catalyzes TG by activating the GPAT1 to catalyze TG synthesis and promote VLDL secretion into the circulation to trigger hyperlipidemia. The gene discussed is SREBF1; the disease is hyperlipidemia.