Haemmerle and colleagues have shown that progressive lipids accumulation and myocardial fibrosis in heart of ATGL-KO mice was accompanied by left ventricular hypertrophy and impaired left ventricular systolic function [10], suggesting that the correct enzymatic activity of ATGL is a limiting condition for the cardiac muscle functionality and homeostasis. The gene discussed is PNPLA2; the disease is left ventricular hypertrophy.