This discrepancy may be attributed to several factors: (a)The biological effects of AFP in P53-mutated subgroups might be masked by concurrent driver mutations (e.g., β-catenin mutations) [26]; (b) Conventional AFP cutoff values (e.g., 400 ng/mL) demonstrate insufficient sensitivity for P53-specific subtyping; and (c) Our cohort predominantly consisted of hepatitis B virus-associated HCC (80%), whereas previous studies mainly focused on hepatitis C-related cases - this etiological difference may lead to distinct AFP expression profiles. This evidence concerns the gene TP53 and hepatocellular carcinoma.