Dysregulation among these nodes—characterized by reduced PLA2G2A and GGT5 expression together with elevated CYP2J2 and EPHX2—may reflect a disrupted AA-EET axis that favors oxidative stress, endothelial dysfunction, and maladaptive cardiac remodeling, ultimately contributing to HF progression (19). The gene discussed is EPHX2; the disease is endothelial dysfunction.