Sudden cardiac death (SCD) is common and affects a heterogeneous group, from those with established cardiovascular disease to a population without structural heart disease and those with malignant inherited arrhythmic syndromes. Worldwide estimates are that 50% of all such deaths are linked to ventricular fibrillation (VF) [1]. In high-risk patients or resuscitated VF survivors, implantable cardiac defibrillators (ICD) are the cornerstone first-line therapy to abort further episodes [2,3]. However, ICDs do not prevent recurrent episodes and, even with antiarrhythmic therapy, up to 20% of patients with ICDs experience recurrent VF episodes and even electrical storms (multiple recurrences of ventricular arrhythmias over a short period of time), with a clear morbidity burden and increased mortality [4,5].Ventricular fibrillation (VF) is a common and life-threatening arrhythmia resulting in sudden cardiac death (SCD). Due to the inherent challenges of mapping VF in humans, the underlying mechanisms that initiate and sustain this common arrhythmia are still poorly understood. In high-risk patients and survivors of SCD, implantable cardioverter defibrillators (ICD) play a central role in treating VF episodes, however, ICDs do not prevent VF recurrences and patients remain at risk of electrical storm and multiple shocks that are often refractory to escalation of medical therapy. More recently, the utility of catheter ablation (CA) has extended to the treatment of VF storms. This review will focus on updates in elucidating the mechanism of VF leading into the role and indication of CA as a treatment strategy.