This difference is likely attributable to several factors: (1) the substantially smaller sample size of the LF group (6.56% prevalence) compared to the NAFLD group (31.15% prevalence), resulting in wider confidence intervals and potentially reduced statistical power; (2) the multifactorial etiology of liver fibrosis, which involves complex interactions between various inflammatory mediators, fibrogenic factors, and genetic determinants beyond the influence of AGP alone; and (3) the possibility that AGP may play a more direct role in hepatic steatosis development compared to fibrogenesis. This evidence concerns the gene ATP5MK and Hepatic steatosis.