To determine whether MTA1 promotes the metastatic behavior of CRC cells by driving mitochondrial glucose metabolism reprogramming, we treated MTA1‐OE cells with the ATP synthase inhibitor oligomycin A. Oligomycin A treatment significantly abolished the increase in the proliferation, colony formation, and invasiveness of HCT116 cells induced by MTA1 overexpression (Figure5A–E), suggesting that MTA1 may promote the malignant behavior of CRC cells by enhancing ATP synthase function. The gene discussed is MTA1; the disease is colorectal carcinoma.