Yuan et al. (2023) found that the expression level of miR-22-3p was significantly upregulated in both CMs-derived exosomes from mice with chronic myocardial infarction and plasma-derived exosomes from patients with heart failure. In vitro studies have confirmed that overexpressed miR-22-3p in exosomes can directly target the acyl-CoA synthetase long-chain family member 4 (gene name: ACSL4) gene of tumor cells, thereby inhibiting cell iron death induced by iron death inducers of Ras and ST, which is one of the important mechanisms of accelerating tumor progression in heart failure. The gene discussed is ACSL4; the disease is heart failure.