Although CXCL4 deletion has previously been shown to be atheroprotective on the Apolipoprotein E null background11, such a broad stroke removes a number of potentially pro-atherosclerotic CXCL4 activities outside of CCR1 signalling, such as promoting oxidised LDL binding to the vasculature and inhibiting oxLDL endocytosis by the LDL receptor40 in addition to T cell recruitment via CXCR3-B17. This evidence concerns the gene APOE and stroke disorder.