Finally, while DOX-treated placebo-injected hearts demonstrated an upregulation of genes involved in fibrosis (Galectin 3) along with fetal and pathological gene expression associated with heart failure (decrease in the myosin heavy chain Myh6/Myh7 ratio, increase in NPPA) compared with DOX-free sham-operated mice (Figures 3G–I), EV-CPC treatment partially prevented these changes conducive to maladaptive remodeling and LV systolic dysfunction (effect size Cohen's d index of 0.4, 0.2 and 0.9 for Galectin 3, Myh6/Myh7 and NPPA respectively). The gene discussed is LGALS3; the disease is heart failure.