Further experimental analysis of Nrf1-/- livers with cholesterol-led increased levels of H2O2 and phosphorylated JNKs, revealed that Nrf1 suppresses cholesterol accumulation and stress-triggering inflammation (NASH) by down-regulated CD36 (and AbcA1, AbcG1, Gltp, ApoC2, F4/80, C1Q8, Orm2, Saa2), but also promotes cholesterol excretion by up-regulated Cyp7a1, Cyp7b1 and Cyp8b1 (besides Ces1f and Insig1), when compared to wild-type controls. This evidence concerns the gene NRF1 and metabolic dysfunction-associated steatohepatitis.