In vivo and in vitro, NCAPD3 could reprogram the glucose metabolism by enhancing glycolysis process and suppressing TCA cycle via both increasing the expressions of c-Myc and E2F1 and recruiting these two transcription factors to the promoters of their target genes, suggesting that NCAPD3 played an important role in regulating glucose metabolism for the occurrence and progression of CRC. This evidence concerns the gene NCAPD3 and colorectal carcinoma.