Recently, by combining advanced flow cytometry and fate-mapping approaches, the same group revisited the model and observed that M2 macrophages accumulated in the reparative phase were derived from Gr1high monocytes during myocardial infarction.14 Our findings are consistent with those of Satoh et al.36 who used mice depleted in M2 macrophages in AT (Trib1−/− mice) and demonstrated that the M2 ATM deficiency was responsible for an increase IR, an increase AT inflammation and, very interestingly, a reduction in fat mass, similar to our findings in CX3CR1−/− mouse female model. The gene discussed is TRIB1; the disease is myocardial infarction.