It has been known for some time that some of the anticancer effects of chemotherapy originate from an immune-based response. Now, researchers have uncovered this mechanism in more detail in a mouse study published in Nature Medicine. The investigators showed that anthracyclines can cause a rapid production of type I interferon by tumour cells that is caused by activation of the Toll-like receptor 3 (Tlr3). The type I interferon molecules are able to trigger autocrine and paracrine signalling loops that release CXC chemokine ligand 10 (CXCL10). Tumours in mice that lacked Tlr3 failed respond to chemotherapy unless type I interferon or CXCL10 was present. Moreover, in several independent patient cohorts who had breast cancer associated with a poor prognosis, a type I interferon-like molecular signature was able to predict clinical response to treatment with chemotherapy.