CXCL9 is a ligand for the receptor CXCR3 and has been shown to promote the infiltration of CD8 T-cells into tumours.40 In addition, the blood plasma levels of CXCL9 in PDAC patients receiving chemotherapy has been shown to correlate with longer overall survival and a longer time to progression.41 Thus, STAT3-depletion reprograms the chemokine secretory profile of FAK-wt and FAK-/- cells in favour of CD8 T-cell infiltration, complementing FAK-dependent reprogramming of antigen processing and presentation pathways required to promote T-cell tumour recognition. The gene discussed is CXCR3; the disease is neoplasm.