The SYNE1 mutations (p.R8272Q, p.S8381C, p.N8406K and p.R374H) increased levels of nesprin‐1α and Lamin A/C protein and disrupted LINC, which contributed to the pathogenesis of DCM (Puckelwartz et al., 2010; Zhou et al., 2017). The gene discussed is SYNE1; the disease is familial dilated cardiomyopathy.