This limitation led to unknown responses to autologous immune cells in preclinical studies and poor prediction of outcomes in human trials.57 In this study, the reason for using autologous PDX/TIL pairs was to stimulate a tumor-specific TIL repertoire which synergized with attIL12-CSV binding to maximize IFNγ production in the sarcoma tumor environment. This evidence concerns the gene IFNG and neoplasm.