Valdivia and colleagues identified an SCN3B mutation V54G in a 20-year-old patient suffering from idiopathic ventricular fibrillation (IVF) and the mutation then caused a functional defect of SCN3B and reduced the sodium current, possibly via the mechanism of interfering with the normal localization of chaperone and cell membrane of SCN3B, thus, confirming that SCN3B, indeed, performs a significantly important role in maintaining the electric stability of the heart [22]. The gene discussed is SCN3B; the disease is ventricular fibrillation.