This putative pro-atherogenic function of the LOX-1 NTF was further validated in a mouse model of atherosclerosis, where SPPL2a/b double-deficient mice subjected to a bone marrow transplantation with wild type bone marrow were treated with a high fat diet after lowering of LDLR levels by overexpression of a PCSK9 gain-of-function mutant. The gene discussed is OLR1; the disease is atherosclerosis.