In this study, we found that knockdown of Arf1 in tumor cells or treatment of mice with the Arf1 inhibitors dramatically suppresses tumor formation by promoting tumor infiltration of cytotoxic T cells via the lyso-phosphatidyl ethanolamine (LPE)-peroxisome proliferator-activated receptor-γ (PPARγ)-nuclear factor-κB (NF-κB)-C-C chemokine ligand 5 (CCL5) pathway. The gene discussed is CCL5; the disease is neoplasm.