The finding that MIAT can absorb miR-24 through its sponge-like action as a ceRNA provided an explanation for the ischemic down-regulation of miR-24 and allowed us to have establish a new fibrosis-regulatory modality MIAT↑ → miR-24↓ → Furin/TGF-β1↑ → cardiac fibrosis↑, which operates in MI and maybe in other cardiac pathological processes associated with fibrosis. The gene discussed is FURIN; the disease is myocardial infarction.