GL-3 accumulation in cardiomyocytes can lead to unexplained, progressive left ventricular hypertrophy (LVH), either as an isolated finding or in conjunction with other Fabry disease symptoms.^2,3 LVH in Fabry disease typically combines concentric thickening with absent or minimal left ventricular obstruction and normal left ventricular ejection fraction. However, asymmetric septal or atypical hypertrophy has also been described, along with subaortic obstruction, which may mimic the phenotypical and clinical features of sarcomeric HCM.³