Given a central role of HLA class I in the restriction of CD8+ CTL recognition of carcinoma-specific antigens, loss of HLA class I expression undoubtedly becomes a major escape pathway for the evasion of CD8+ CTL surveillance, by which any HLA class I deficient carcinoma variants can develop to more aggressive or invasive phenotypes without stimulation of primary anti-carcinoma immunity, CD8+ T cell response. The gene discussed is CD8A; the disease is carcinoma.