Since both HMOX1 and UGT1A1 are involved in the defense against increased oxidative stress, we had aimed to assess whether the genetic variations associated with either enhanced HMOX1 activity (responsible for increased bilirubin production), or decreased UGT1A1 activity (responsible for sluggish bilirubin biotransformation), are less prevalent in NAFLD patients. Here, HMOX1 is linked to metabolic dysfunction-associated steatotic liver disease.