Our study indicates that an increase in TCA cycle metabolites could be due to the increased glycolytic flux, which is characteristic of colon cancer.53 Consistent with this hypothesis, loss of the TSP1 receptor CD47 altered both glycolytic and TCA cycle flux in a human T-cell line and cd47−/− mice.21 However, the present results suggest decreased TCA cycle activity and oxidative phosphorylation. This evidence concerns the gene CD47 and colonic neoplasm.