Lefeber et al. [41] have described different pathogenic mutations in the DOLK gene in 11 young patients with predominantly nonsyndromic DCM and showed that dolichol kinase loss determines abnormal N-glycosylation and a reduction of the O-mannosylation of α-dystroglycan, leading to DCM. The gene discussed is DAG1; the disease is familial dilated cardiomyopathy.