The molecular determinants driving SSA/Ps appear to be distinct from those of conventional adenomatous polyps, which instead of following the “adenoma to carcinoma pathway”, are characterized by genetic/epigenetic changes in the B-Raf Proto-Oncogene, Serine/Threonine Kinase gene (BRAF) and a form of epigenetic instability more commonly referred to as the CpG island methylator phenotype (CIMP; reviewed in [42,43]), which is expected to promote the epigenetic silencing of numerous genes with pathogenic implications. This evidence concerns the gene BRAF and adenoma.