Nevertheless, these findings were not supported by a correlation between NAFLD-associated fibrosis and the levels of syndecan-1, as in the case of fibrosis due to hepatitis C. A possible explanation for this discrepancy is represented by the presence of different risk factors for hepatitis C-induced fibrosis (insulin resistance and virus-induced liver inflammation), compared with the factors that facilitate fibrosis in patients with NAFLD (steatosis and systemic inflammation). This evidence concerns the gene SDC1 and metabolic dysfunction-associated steatotic liver disease.