Notwithstanding their apparently different inflammation modulatory functions and the contribution of the cell type, the similarity between ICP10PK and H11/HspB8 suggests that they may contribute to the onset of autoimmunity through “molecular mimicry.” Indeed, linear peptide epitopes, processed from viral proteins, mimic normal host self-proteins, thus leading to an immune cross-reaction between the virus and host cell antigens, with inflammation as a typical sign of autoimmune diseases [69, 70]. This evidence concerns the gene H1-1 and Autoimmunity.