Amyloid deposition, also known as systemicamyloidosis, is a disease that disrupts cellular and organ function due to the deposition of amyloid in the interstitial spaces of extracellular tissues throughout the body, as recently defined by Picken et al. It is a syndrome of amyloid deposition due to abnormal folding of protein molecules caused by different factors such as genetic degeneration and infection. The clinical manifestations are heterogeneous because the deposited amyloid protein and the affected organs vary. The common organs involved are liver, kidney, nerves, heart, gastrointestinal tract, etc. The skin, tongue, and lymph nodes are the most commonly involved tissues. All tissues and organs of the body can be involved, but not necessarily with clinical manifestations. The differential diagnosis of amyloid deposition should be divided into two steps: the first step is the differentiation of amyloidosis from other diseases; the second step is the differentiation of the type of amyloidosis after the diagnosis of amyloidosis is confirmed, because different types of amyloidosis differ in terms of treatment and prognosis, so the differentiation of the type of amyloidosis has important clinical significance, which is easily ignored. Amyloid deposition has a chronic course and occurs mostly in middle-aged and elderly people. The possibility of amyloidosis should be considered for unexplained chronic organ enlargement and/or insufficiency in middle-aged and elderly people, especially for unexplained multi-organ enlargement and insufficiency (heart, kidney, liver, spleen, tongue, etc.), which should be included as one of the differentiating diseases. Because the clinical manifestations of this disease are not specific, the exclusion method is often used, i.e., for organ enlargement and insufficiency for which no clear cause can be found, this disease should be listed as one of the diseases that must be excluded, and the final diagnosis depends on the pathological examination of biopsies. When the pathological examination of biopsies (light microscopy, Congo red staining and polarized light detection) confirms amyloidosis, the type of amyloidosis should be identified, and the identification of the type of amyloidosis is based on the clinical features and biochemical characteristics of the amyloidogenic material (protein). Basically, hemodialysis-related amyloidosis, familial Mediterranean fever, familial polyneuropathy, senile amyloidosis, central nervous system amyloidosis and restrictive amyloidosis can be excluded, and primary systemic amyloidosis, systemic amyloidosis associated with multiple myeloma and secondary systemic amyloidosis should be considered. Patients with systemic amyloidosis associated with multiple myeloma should have clinical manifestations of myeloma (bone pain, anemia, infection, hyperviscosity syndrome, hypercalcemia, etc.), myeloma cells visible on bone puncture, osteolytic lesions visible on X-ray, and M protein visible on protein electrophoresis, so it is not difficult to distinguish them from primary systemic amyloidosis, while secondary systemic Secondary systemic amyloidosis is mostly secondary to chronic infectious diseases (tuberculosis, osteomyelitis, bronchiectasis, leprosy, etc.) or chronic inflammatory diseases (e.g. rheumatoid arthritis, Schegren’s syndrome), with clinically significant manifestations of the primary disease (infection or inflammation), which can be distinguished. AA protein, which can be distinguished by applying enzyme-labeled or fluorescence-labeled monoclonal antibody detection.