This latter observation mirrors the circumstance presented in several reports on cytotoxic CD4+ T cells, although our data extend the context of this observation by showing that endogenous expression of the source antigen and induction of MHC-II by IFN-γ is unlikely to yield a physiologic target on epithelially derived tumor cells for TCRs against nuclear or membrane-associated antigens. This evidence concerns the gene CD4 and neoplasm.