In bacterial sepsis, PF4 binds to glycosaminoglycans (GAGs) on the surface of aerobic bacteria, forming an antigenic complex that may induce early generation of anti-GAGs/PF4 IgA-IgG-IgM [5,6] as a defense mechanism, prompting phagocytosis and contributing to innate immunity [7] and autoimmunity [8]. This evidence concerns the gene CD79A and bacterial infectious disease with sepsis.