A 48-year-old fit and healthy medical personnel was in his typical state of health when he suddenly collapsed in his clinic. Resuscitation manoeuvres were performed by the mobile emergency medical unit, and they promptly recognized ventricular fibrillation. The patient was successfully resuscitated. He had no previous medical history nor any symptoms of angina, palpitation, fever, respiratory tract infection, or syncopal/pre-syncopal attacks prior to the event. He has no previous history of SCD or young onset of cardiovascular disease in the family. He was not on any traditional supplements/medications. Cardiovascular examination revealed a pansystolic murmur best heard over the mitral area radiating to the axilla. Other clinical examinations were unremarkable. Blood investigations ruled out infective, acute ischaemic, and toxicological causes. Electrocardiogram post-resuscitation revealed premature ventricular contraction with no evidence of pseudo-right bundle branch block, prolonged QT, delta, or epsilon waves (). A transthoracic echocardiogram and cardiac MR showed features of Barlow’s disease. The transthoracic echocardiogram showed bileaflet MVP, a MAD measuring 1.2 cm, a moderate mitral regurgitation, a dilated mitral valve annulus measuring 4.5 cm, and a normal left ventricular size with normal systolic function with a left ventricular ejection fraction of 58%. There was no gross regional wall abnormality. The cardiac MR also showed MAD (), thickened valves, bileaflet prolapse, and dilated mitral valve annulus. The late gadolinium enhancement () revealed inferior and inferolateral ventricular wall fibrosis. There was no evidence of acute myocardial inflammation or oedema. Being a young patient with no previous medical illness, to obtain more information on this unexplained cardiac arrest, we performed whole genome sequencing and found mutations in the CACNB2 genes (Chr10: 18150879 and Chr10: 18539538 variants). Single coil electrode dual-chamber ICD implantation was offered as a secondary prevention, as subcutaneous ICD (S-ICD) was unavailable in our centre at the time (). During the 6-monthly follow-ups, the ICD check showed only multiple frequent premature ventricular contractions. The work on offspring’s genetic screening for mutations in CACNB2 genes after obtaining a written informed consent in the pre-test genetic counselling sessions is currently ongoing.