The “traditional” pathway, the so-called adenoma-carcinoma-sequence, described by Vogelstein and colleagues in the early 1990s, is characterized by an early bi-allelic inactivation of APC caused by alterations in the mutation cluster region (codons 1243–1567) of this gene followed by an oncogenic K-Ras codon 12 or 13 mutation, inactivation of the tumor suppressor gene Tp53 at the transition from adenoma to carcinoma [1-3] and chromosomal instability [4]. Here, APC is linked to carcinoma.