Exosomes from hypoxic cardiomyocytes exacerbated cardiac dysfunction, cardiac fibrosis, and myofibroblast differentiation in post-MI rats and caused cardiac miR-208a levels to be increased, with post-MI cardiac dysfunction and fibrosis being driven by miR-208-mediated targeting of the differentiation-regulating factor Dyrk2 [170]. The gene discussed is DYRK2; the disease is myocardial infarction.