Complementary experiments suggested that in experimentally induced RA, these anti-TNF-a auto-Abs participate in the natural regulation of disease and restrain—although they are incapable of totally preventing—its development (3). Nevertheless, their selective amplification by targeted DNA vaccines led to rapid recovery from an ongoing disease (8). These studies also showed that selective breakdown of tolerance to TNF-a is due to its preferential expression at a partially immune-restricted site undergoing a destructive process (3, 8). Very recently, we have shown that type I diabetes mellitus (T1DM) patients preferentially display auto-Ab production to CCL3( Chemokine (C-C motif) ligand 3) and not to several other proinflammatory chemokines (9).