The main pathophysiological mechanism of NAFLD involves increases in FA accumulation and decreases in mitochondrial FA oxidation that lead to hepatocyte lipid metabolism dysfunction and lipid accumulation and to hepatocyte injury resulting from activation of tumor necrosis factor-ɑ and stimulation of reactive oxygen species (ROS) production (Berlanga et al. 2014). The gene discussed is TNF; the disease is metabolic dysfunction-associated steatotic liver disease.