The protective effects of various molecules and drugs on pathological myocardial hypertrophy depend on the modulation of ceramide, the overexpression of fat triglyceride lipase (ATGL), the rate-limiting enzyme of triglyceride (TG) hydrolysis, increases PPARα activity, which results in the enhancement of FA oxidation, reduction of ceramide, and prevention of pressure overload-induced cardiac hypertrophy [68]. This evidence concerns the gene PPARA and cardiac hypertrophy.