Here its role has been rather ambiguous, with some reports stating that acute exposure of tumour cells to high levels of IFN‐I result in growth arrest and cell death, and others stating that chronic exposure to low levels of IFN‐I might aid tumour survival and immune‐evasion Further, secretion of IFN‐I was shown to also lead to increased concentrations of CXCL9 and CXCL10 within the TME, CCL3 and CCL5 in the spleen, promoting the recruitment of NK and CD8+ T cells to these sites [26, 36, 37]. The gene discussed is CXCL9; the disease is neoplasm.