In animal model of MI, silencing of miR-34 family attenuates MI-induced pathological left ventricular remodeling after MI and improves cardiac function by suppressing vascular endothelial growth factors (VEGF), vinculin, protein O-fucosyltransferase 1 (Pofut1), Notch1, and semaphorin 4B (Sema4b) [172]. The gene discussed is VCL; the disease is myocardial infarction.