However, as our population exhibited relatively mild hepatic disease, the surrogate endpoints assessed by MRI, along with the measurement of serum CK-18 and P3NP levels as validated biomarkers of hepatic damage and fibrogenesis in the course of NAFLD [26, 27, 31], can be considered suitable for this phase of the study. This evidence concerns the gene KRT18 and metabolic dysfunction-associated steatotic liver disease.