Similarly, IRF5 silencing via siRNA in ApoE-/- mice results in decreased M1 macrophages and accelerated wound healing after myocardial infarction, whereas transgenic absence of IRF5 gene (i.e., ApoE-/- IRF5-/- double knock-out) results in decreased necrotic core formation [12,13]. Here, APOE is linked to myocardial infarction.