Specifically, using a rodent model of heart failure, the group of Dr. Suzuki showed that extracellular HMGB1 contributed to the protective effects exerted by bone marrow mononuclear cells (BMCs) following transplantation in the failing myocardium by modulating macrophage’s polarization towards the anti-inflammatory M2 phenotype [85]. This evidence concerns the gene HMGB1 and heart failure.