Therefore, we found that: (1) the knockdown of Arf1 dramatically blocked the tumorigenic capability of CT26 and B16-F10 cells; (2) the knockdown of Calr or HMGB1 or BiP significantly reduced the anti-tumor activity of Arf1 knockdown; (3) treatment with the ER stress inhibitor PBA or GSK2606414 significantly blocked the anti-tumor activity of Arf1 knockdown while treatment with ER stress inducer Tunicamycin significantly enhanced the anti-tumor activity of Arf1 knockdown; and (4) the knockdown of ERp46 did not significantly change the anti-tumor activity of Arf1 knockdown. This evidence concerns the gene DDX53 and neoplasm.