Several animal studies have demonstrated that even low-level exposure to mercurials induces autoimmune vasculitis in susceptible rodent strains [64,65,66], which is characterized by T cell-dependent polyclonal activation of B lymphocytes, marked increases of serum immunoglobulins such as IgE and proinflammatory cytokines such as TNFα, detectable antinucleolar autoantibodies (ANoA), and widespread vascular immune complex deposition that may also be specific to various target organs such as in Hg-induced glomerulonephritis [67,68,69,70]. This evidence concerns the gene IGHE and glomerulonephritis.