A 1976 vision of possible models to explain the clonality of virus-immune, cytotoxic, thymus-derived lymphocytes associated with H-2K or H2-D. The lack of knowledge at that time of the structure and specificity of the T-cell receptor and of the ability of antigenic peptides to fit in the groove of major histocompatibility complex (MHC) antigens made it very difficult to interpret the data showing a similarly restricted recognition of viral and tumor-associated antigens and those indicating the ability of tumor antigens to be cross-presented on autologous MHC antigens different from those expressed on the immunizing tumor cells [4]. Only the models depicted in (i)a and (ii)a represented a rudimental and much approximated vision of the present understanding of T-cell antigen recognition. The knowledge of the specificity and control of T-cell–mediated immunity, as well as the role of inflammation and innate resistance to both regulate adaptive immunity and tumor initiation and progression, has since allowed great advances in the understanding and translational utilization of the shared immune mechanisms between infection and cancer. Reproduced with permission from the article by Doherty et al [5].