Introduction Familial dilated cardiomyopathy (Familial DCM) is a result of a genetic mutation in one or more of the 50+ identified genes, which encode components of the cardiac cytoskeleton, sarcomere and nuclear lamina. Genes associated predominantly with arrhythmogenic DCM include TTN (encodes titin), LMNA (encodes lamin A/C), FLNC (encodes filamin C) and SCN5A (encodes sodium voltage-gated channels). Early diagnosis of arrhythmogenic DCM genotypes can impact clinical management including earlier prophylactic defibrillator (ICD) implantation and referral for cardiac transplantation. Familial DCM continues to be under-recognized with recent studies suggesting a familial component in up to 25-40% among nonischemic cardiomyopathy (NICM) patients. Case Report A 54-year-old male presented to ER with recurrent, symptomatic, hemodynamically stable monomorphic ventricular tachycardia (VT) despite his metoprolol succinate, amiodarone and mexiletine therapies. His medical history includes ventricular fibrillation in 2012 (in the absence of coronary artery disease (CAD)) status post single chamber ICD, history of atrial fibrillation in 2018 status post radiofrequency ablation, dilated cardiomyopathy with moderately reduced ejection fraction with NYHA class II symptoms with CRT upgrade in 2019 and hypertension. Family history notable for presumed NICM in his father who underwent cardiac transplantation. Patient underwent a thorough cardiac evaluation with non-obstructive CAD on coronary angiogram and no myocardial inflammation on cardiac PET. Despite the addition of intravenous antiarrhythmic therapies and two successful endocardial and epicardial ablations (using unipolar and bipolar methods) of the anterobasal LV, his clinical VT persisted. He then underwent a bilateral stellate ganglion block followed by a surgical sympathectomy, yet his VT remained refractory. Genetic testing revealed mutations in the MYBPC3 and TTN genes. Based off his clinic history and high-risk genetic predisposition, a repeat ablation was not pursued and instead a transplant evaluation was initiated. Two weeks later, the patient underwent an uncomplicated cardiac transplant. Summary A familial component is often identified in NICM patients with confounding ventricular arrhythmias. The presence of arrhythmogenic genetic variants may identify those who benefit more from advanced heart failure therapies versus aggressive ablation attempts.