For instance, in a mouse model of spontaneous bone metastasis, genetic silencing of IRF7 significantly promotes breast cancer bone metastasis via immune escape 28; in lung cancer cells, knockdown of IRF7 increases sensitivity to oncolytic viruses 29; moreover, IRF7 deficiency leads to significant accumulation of granulocytic myeloid-derived suppressor cells (G-MDSCs), and therefore promoted tumor growth and metastasis in mice 30. Here, IRF7 is linked to neoplasm.