Multiple Sclerosis (MS) is an autoimmune disease that leads to widespread pathology within the central nervous system (CNS) and is the most common cause of neurologic disability among young adults within the US. Pathologic descriptions of multiples sclerosis have documented damage to the myelin sheath around axons and to underlying neurons. The mechanism of damage has long been ascribed to auto reactive T cells that infiltrate the CNS and cause tissue injury. Over the last decade, however, a significant amount of data has implicated a deranged B cell biology in the pathogenesis of this disabling condition. Work completed within labs at UT Southwestern have identified a novel pattern of somatic hypermutation among B cells from MS patients. This pattern is currently being studied as a potential new biomarker or diagnostic test for the condition. Continued research has begun to determine the antigenic targets of this deranged B cell biology and will point the field in new research directions. This presentation will present data relative to the identified pattern of somatic hypermutation from MS patients, the biology of the produced antibodies from these unique cells and implications for future research.