Furthermore, the administration of D6D inhibitors prevents remodeling of FA composition and attenuates myocardial elevations in pathogenic eicosanoid species and lipid peroxidation to suppress cardiac hypertrophy, fibrosis, and contractile dysfunction [36,37], indicating that aberrant activation of FADS2 has a pathogenic role that exacerbates heart failure through unwanted desaturation of FAs. The gene discussed is FADS2; the disease is cardiac hypertrophy.