It remains unclear how autoantibody production occurs in patients with autoimmune disease despite self-tolerance mechanisms. Cryoglobulinemic vasculitis is an autoimmune pathology frequently associated with chronic hepatitis C virus (HCV) infection, whereby patients develop a precipitating cryoglobulin composed of monoclonal IgM rheumatoid factor bound to polyclonal IgG. Previous work by our lab has shown somatic variants associated with B cell lymphomas or leukemias can be found in B cells isolated from Sjögren's syndrome patients with cryoglobulinemic vasculitis. Using bulk and single cell next generation sequencing techniques, we have deeply analysed an expanded “rogue” B cell clone in a HCV patient with cryoglobulinemic vasculitis, to reveal similar findings. Whole genome sequencing has identified somatic gene variants specific to the rheumatoid factor cryoglobulin-producing B cell clone, which are absent from the polyclonal B cells of the patient. Certain somatic variants identified provide functional insight into how the rogue pathogenic autoantibody-producing B cell may be persisting. Furthermore, by reconstructing and expressing rogue B cell clone antibody sequences to measure precipitating capacity and specificity to IgG or HCV antigens, we have extrapolated a possible somatic hypermutation pathway taken by the rogue B cell clone leading to rheumatoid factor and cryoglobulin activity. Our findings related to this particular “rogue” B cell clone may have broader implications for autoantibody production in other autoimmune conditions.