This process triggers an avalanche of many factors such as an increase in the activity of cytochrome P450, an increase in the production of reactive oxygen species, lipid peroxidation, a deficiency in antioxidant defense, activation of proinflammatory cytokines and the nuclear transcription factor NFκB, and an increased expression of PPAR receptors, initiating the transition from steatosis to steatohepatitis. The gene discussed is NFKB1; the disease is steatosis.