ALCAT1-mediated CL pathological remodeling can accelerate reactive oxygen species (ROS) generation and CL oxidation, resulting in reduced CL content and consequent mitochondria-induced apoptosis in various conditions such as myocardial hypertrophy, heart failure, diabetes, aging, obesity, and other diseases [10,12,31,32]. This evidence concerns the gene LCLAT1 and cardiac hypertrophy.