To confirm whether the activated IFN‐I signaling is mediated via the IFN‐I receptor IFNAR, we generated IFNAR1−/− MB231 and MCF7 cells using CRISPR‐Cas9 technology and found that DC with BM‐MSCs could no longer increase HLA‐I expression (Figure 5B) or induce NK resistance in the IFNAR1−/− cancer cells (Figure 5C) compared to that in WT cancer cells. The gene discussed is IFNAR1; the disease is cancer.