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. The gene discussed is PNPLA2; the disease is obesity due to melanocortin 4 receptor deficiency.