Short-term elevations of FGF21 during hypertension, ischemia–reperfusion injury, and β-adrenergic activation have been shown to be cardioprotective [63,64,65,66,67,68,69,70] and prevent pathologic cardiac hypertrophy through the activation of FGFR1c/β-klotho [71,72], promoting antioxidant gene expression and inhibiting the formation of reactive oxygen species [73]. The gene discussed is FGF21; the disease is cardiac hypertrophy.