Having identified that Psmb8 was important for regulating the growth of FAK-/- tumours (figure 3G) and that the FAK-/- tumour growth defect was CD8 T-cell-dependent (figure 1C), we postulated that increased expression of both Psmb8 and H2-Kb in response to co-depletion of FAK and STAT3 might further restrain tumour growth and potentiate the antitumour CD8 T-cell response. This evidence concerns the gene STAT3 and neoplasm.