In conclusion, our data demonstrate a dysregulated metabolism of bilirubin in adult NAFLD patients, most likely due to increased oxidative stress accompanying NAFLD, since the frequencies of the major functional variants in the HMOX1 or UGT1A1 gene promoters did not demonstrate to have any major effect on development of NAFLD. This evidence concerns the gene HMOX1 and metabolic dysfunction-associated steatotic liver disease.