To define the effects of PCSK9 on the regulation of plasma apoB and atherogenesis more precisely, and to determine to what extent these effects may be LDLR dependent, the Pcsk9 gene was deleted from our atherosclerosis-prone mouse model, Ldlr−/−Apobec1−/− (LDb) (11, 16–19), which lacks both LDLR and Apobec1, to produce a Ldlr−/−Apobec1−/−Pcsk9−/− (LTp) triple KO mouse. The gene discussed is LDLR; the disease is atherosclerosis.