90 In addition, mice with liver-specificMT1-MMP deletion have increased LDLR in the liver, but lower plasmalevels of soluble LDLR, in association with a reduction in plasmacholesterol levels.90 Given that furinis responsible for the MT1-MMP maturation,91 an increase in furin activity might elevate plasma LDL-C levelsby promoting LDLR shedding (Figure 4).90 Although PCSK9 is anotherfurin substrate,92,93 furin-cleaved PCSK9 remains activein LDLR degradation and cholesterol catabolism.94 Therefore, PCSK9 might not be a primary target of furinin promoting dyslipidemia. The gene discussed is LDLR; the disease is metabolic syndrome.