Additionally, because hypoxia-invoked HIF-1α activation transcriptionally regulates LBH expression [29], we hypothesize that the ascending LBH level observed in CFs in the post-MI cardiac microenvironment might be partially independent of TGF-β1-related induction during the inflammatory phase, when LBH proteins could be transferred from LBH-upregulated hypoxic CMs as we proved. The gene discussed is TGFB1; the disease is myocardial infarction.