Recent progresses in molecular biology have allowed us to identify at least two different molecular mechanisms implicated in colorectal carcinogenesis: chromosomal instability and genetic instability. These two molecular mechanisms are supported by two hereditary syndromes that predispose to colorectal cancers: familial adenomatous polyposis and hereditary non polyposis colorectal cancer syndrome. In spite of these two different mechanisms, the signalling pathways implicated the malignant transformation of colonic epithelial cells seem to be the same. They are essentially represented by APC/beta-catenin, TGFbeta, RAS and TP53 signalling pathways. This new molecular classification of colorectal cancers is important for the understanding of molecular alterations responsible for tumour development but also for the management of patients.