Importantly, DDX39B augmented the Warburg effect by nuclear PKM2-dependent transcription, supporting the expression of GLUT1 and LDHA and leading to increased glucose uptake and lactate production and eventually the initiation and development of CRC, as a constitutively cytosolic PKM2 mutant (R399/400A) reversed the DDX39B-mediated enhanced proliferation and migratory ability of CRC cells. This evidence concerns the gene PKM and colorectal carcinoma.