This notion is derived from our novel findings that (1) increased gut microbial components and products translocation into the systemic circulation conduce to inflammation post-MI, (2) the increase of gut bacterial translocation products has great prognostic significance for cardiovascular outcomes, (3) the loss of occludin and intestinal mucosal injury is responsible for elevated gut permeability and microbial translocation post-infarction, and (4) cardiomyocyte injury post-infarction could be alleviated dramatically by gut microbial translocation inhibition. This evidence concerns the gene OCLN and infarction.