Data demonstrate that extracellular ASC specks, independent of IL-1β, govern the pathogenesis and extent of amyloid A (AA) amyloidosis, which is characterized by deposition of insoluble amyloid fibrils in tissues and organs disrupting their structure and function.Extracellular ASC interacts with serum amyloid A (SAA) released by the liver during inflammation, forming a scaffold that accelerates SAA aggregation into amyloid fibrils, which are deposited in tissues and organs.Amyloid A amyloidosis occurs in a heterogeneous spectrum of chronic inflammatory conditions such as rheumatoid arthritis, Crohn's disease, and inflammatory bowel disease.ZyVersa is developing Inflammasome ASC Inhibitor IC