Because the secretory PCSK9 protein is also produced by the intestine and other tissues (Zaid et al., 2008), we hypothesized that conditional knockdown of hepatic PCSK9 could attenuate hyperlipidemia-induced liver inflammation as PCSK9 secreted by extrahepatic tissues is transported to the liver, thereby partially compensating PCSK9 deficiency. The gene discussed is PCSK9; the disease is hyperlipidemia.