We examined whether NF-κB regulated the transcription of CCL5 or not in tumor cells with Arf1 inhibitor treatment or Arf1 knockdown, and found that inhibiting Arf1 significantly upregulated the phosphorylation level of p65 protein (p-p65) in CT26 cells (Fig. 5a, Supplementary Fig. S5a). The gene discussed is CCL5; the disease is neoplasm.