Importantly, the increase of LVESd and LVEDd, and the decrease of LVFS, were smaller in the CEACAM1 KO-MI group than in the WT-MI group (P < 0.01, Fig. 3D,E), suggesting that knock-out of CEACAM1 alleviates LV remodeling and dysfunction after MI. This evidence concerns the gene CEACAM1 and myocardial infarction.