Natural history studies have demonstrated that pathogenic variants in DCM-associated genes, such as lamin A/C (LMNA), filamin C (FLNC), cardiac sodium channel NAv1.5 (SCN5A), and RNA binding motif protein 20 (RBM20), lead to a malignant arrhythmogenic phenotype, which can be unrelated to the degree of left ventricular (LV) dysfunction [1]. Here, LMNA is linked to familial dilated cardiomyopathy.