Over 80% CRC have mutations in APC, β-catenin, or axin, which will successively lead to nuclear β-catenin accumulation, TCF/LEF transcription activity augmentation, and increased target genes expression (such as CCND1 and c-Myc), finally resulting in uncontrolled proliferation7,19. The gene discussed is HNF4A; the disease is colorectal carcinoma.