Emerging evidence indicates that GSK-3β is instrumental in modulating lipid metabolism within the heart, especially under conditions of high fat stress [71], and elucidated that in obesity-induced cardiomyopathy, activation of GSK-3β dampens the expression of adipose triglyceride lipase (ATGL) through post-translational regulation of FoxO1. This evidence concerns the gene PNPLA2 and Obesity.