Consequently, ATP-consuming biosynthetic processes would be turned off, ATP-generating catabolic processes turned on35, and antioxidant responses ushered that directly counteract and thus attenuate the concurrent pro-NAFLD/NASH scenario induced by hepatic CYP2E1-ROS-JNK1-activation. This evidence concerns the gene CYP2E1 and metabolic dysfunction-associated steatotic liver disease.