Based on the information presented above and our results in previous studies, we hypothesized that in the peri-infarct myocardium, upregulated LBH in CMs during the inflammatory phase might be involved in LBH-CRYAB-mediated CF proliferation, differentiation into myofibroblasts (MCFs), and epithelial-mesenchymal transition– (EMT–) like processes through intercellular communication in the post-MI cardiac microenvironment, and our investigation in this study focused on CM exosome secretion. The gene discussed is CFTR; the disease is myocardial infarction.