In summary, activation of primary human CTL expressing a recombinant TCR by interaction with tumor target cells could be effective yet was more often limited by low expression of tumor-associated antigens in the target cells, the only moderate affinity of the TCR for the peptide/MHC complexes and limited TCR expression when using an additional disulfide bridge to stabilize the recombinant TCR. The gene discussed is HLA-C; the disease is neoplasm.