Finally, to determine whether the elevated baseline HMGCR activity in PcntSMC–/– SMCs was responsible for the increased atherosclerotic plaque burden observed in Pcnt-deficient mice, male WT and PcntSMC–/– mice were injected with AAV-PCSK9DY to induce hyperlipidemia at age 6 weeks, and then placed on an HFD and 50 mg/kg body weight/day pravastatin in the drinking water for 12 weeks, starting at age 7 weeks. The gene discussed is HMGCR; the disease is hyperlipidemia.