This is followed by Kirsten rat sarcoma viral oncogene homolog (KRAS) activating mutation, promoting adenoma growth; loss of heterozygosity at chromosome 18q (a tumor suppressor loci), due to chromosomal instability, a condition of malfunctioning segregation of sister chromatids during mitosis, allowing adenoma progression; and inactivation of the tumor-suppressor gene p53, which triggers the final transition to carcinoma (20, 23, 24). Here, KRAS is linked to neoplasm.