For example, in autoimmune anti-glomerular basement membrane (anti-GBM) GN or Goodpasture’s disease, where autoimmunity develops against the non-collagenous domain of the α3-chain of type IV collagen (α3[IV]NC1), antigen-specific regulatory CD4+ CD25hi T cells, capable of suppressing Th1 responses, were absent during active disease but significantly elevated during remission and might be responsible for the rarity of relapses in anti-GBM disease (Salama et al. 2003). This evidence concerns the gene CD4 and Autoimmunity.