Light chain (AL) amyloidosis is a complex and often fatal disease caused by misfolded protein deposition characterized by monoclonal immunoglobulin light-chain fibrils in tissues and organs (1). This light chain protein, usually produced by a small and indolent plasma cell clone, is responsible for positive staining with Congo red when observed under polarized light, a gold standard for the diagnosis of AL amyloidosis (2). According to the extent of the amyloid deposits involved, AL amyloidosis classified into the localized AL amyloidosis which only involving single tissue or organ, and the systemic AL amyloidosis which may affect all organs of the body except for central nervous system and generate a wide range of clinical symptoms (3). System amyloidosis is the most common type in western countries, with an estimation of about 9 cases per million inhabitants per year (4). There is a consensus that AL amyloidosis patients with hypercalcemia, renal failure, anemia, and lytic bone lesions due to clonal expansion of plasma cells (CRAB criteria) show the high possibility of concurrent MM.