Emerging evidence also suggests that NAFLD, especially in its necroinflammatory form, might be involved in the pathogenesis of cardiac function abnormalities through the systemic release of several mediators from the steatotic and inflamed liver (including C-reactive protein, interleukin-6, tumor necrosis factor-α, and other proinflammatory cytokines) [11, 55]. The gene discussed is CRP; the disease is metabolic dysfunction-associated steatotic liver disease.