Case Report: A 67-year-old woman presented to our hospital with edema and severe liver dysfunction. Biochemical examination showed AST: 67, ALT: 35, ALP: 2056, GGTP: 124, T-BIL: 1.5, ALB: 2.5, ChE: 90, HPT: 50, PLT: 27.5x104, NH3: 236. HBV and HCV were negative. IgM elevated to 4094 (normal: 60-250). IgG and IgA were normal. HLA-DR4 was positive. Antinuclear antibody and antimitochondrial M2 antibody were negative. CT reveled hepatomegaly with low density on arterial phase imaging. Splenomegaly and collateral blood flow were not observed. Progressive biliary fibrosis, such as PBC or PSC, was suspected. However, ERCP showed no evidence of PSC. Sinusoidal amyloid-depositions with positive Congo Red staining and strong atrophy of hepatocytes were diffusely observed in liver histology. Fibrotic changes, such as an enlargement of portal region or bridging fibrosis, were not found. Cardiac and renal dysfunctions did not exist. Brain MRI showed no abnormal findings. AL hepatic amyloidosis, which demonstrated severe hepatic dysfunction, was diagnosed. Serum IgM-kappa was detected. Kappa free light chain elevated to 168.00 (normal: 2.42-18.92). Serum IL-6, IL-8 levels elevated to 36.9, 69.1 (normal: < 2.41, < 8.0, respectively). Serum markers related to liver fibrosis, P-III-P and type IV-collagen 7S, were normal levels (0.6, 3.2, respectively). However, Mac2-binding protein (M2BPGi), a novel biomarker of liver fibrosis, elevated to 6.35 (normal: < 1.00). Transient elastography (TE) revealed transcended 75.0 kPa of liver stiffness (E), which is a maximum level (normal: < 6.0). Discussion: Amyloid deposition in the liver directly impairs hepatic metabolism. Mechanism of liver damage caused of hepatic amyloid deposition is completely different from process of liver fibrogenesis. TE is a very useful device for liver stiffness measurements. However, to our knowledge, its usefulness for amyloid deposition in the liver has never been reported. Interestingly, TE showed transcended maximum E level despite absence of liver fibrosis. Of note, an elevated serum M2BPGi was found despite normal levels of P-III-P and type IV-collagen 7S. Conclusion: Our present case indicates TE and serum M2BPGi may be novel useful tools to predict hepatic amyloid deposition in AL amyloidosis patients. Further data accumulation, including transient elastography and serum M2BPGi in AL amyloidosis patients, is essential to understand the pathogenesis of AL hepatic amyloidosis.