Various pathogenic mechanisms have been suggested as possible explanations for accelerated atherosclerosis and increased CVD burden in NAFLD patients, including a high oxidative stress state due to steatosis-stimulated fatty-acid oxidation in the liver [23], systemic release of proatherogenic molecules like tumor necrosis factor-α, interleukin-6, and oxidized LDL cholesterol [24], increased IR [25], and macrophage activation [26]. The gene discussed is TNF; the disease is metabolic dysfunction-associated steatotic liver disease.