This effect may be explained by the regulatory function of the nuclear factor erythroid 2-related factor 2 (NRF2) signaling, which is known to limit the progression from NAFLD to NASH by activating genes that promote the elimination of ROS and electrophiles derived from lipid peroxidation and mitochondrial dysfunction [34]. The gene discussed is NFE2L2; the disease is metabolic dysfunction-associated steatotic liver disease.