Fibroblast‐derived exosomes enriched with miR‐27a are transported into cardiomyocytes, where they inhibit PDLIM5 expression and exacerbate cardiac hypertrophy in MI‐induced CHF models, a process closely linked to oxidative stress, which significantly contributes to cardiomyocyte dysfunction and myocardial hypertrophy in CHF [63]. The gene discussed is PDLIM5; the disease is congestive heart failure.