CXCR3 and neoplasm: The approach is also attractive as it may allow anti-tumour responses to access a CXCR3-chemokine dependent amplification loop whereby local CXCR3 ligand expression in the TME (potentially induced by non-specific OV-mediated IFNγ release or by recombinant engineering) promotes the additional recruitment of CXCR3+ CAR T-cells, which in turn secrete IFNγ locally activating the transcription factor STAT1 in TME resident cells further amplifying the infiltration of CAR T-cells [209].