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]. This evidence concerns the gene NFE2L2 and metabolic dysfunction-associated steatohepatitis.