Thus, exposure to infection or other stressors induces expression of HSP65 on the surface of endothelial cells, and this results in a cross-reaction between antibodies produced against MTB HSP65 and self-antigens HSP60 in the host [19,20]. Xu et al. conducted a study on 120 white rabbits with normal serum cholesterol; they were grouped and inoculated with six antigens and adjuvants, one of which was HSP65. The gene discussed is HSPD1; the disease is infection.