CXCR3 and neoplasm: As further demonstrated, Ifnar1−/− tumor cells failed to secrete CXCL10 in response to doxorubicin, just as was also seen in tumor cells derived from Tlr3 KO or its adaptor Trif. These data demonstrated that ICD inducers act by stimulating IFN-β secretion through an autocrine and paracrine mechanism that takes place upon TLR3 recognition of self RNA from dying cells, activating the CXCL10-CXCR3 signaling axis to attract effector immune cells [293].