The initial event in the development of CRC and the formation of polyp is the inactivation of the APC tumor suppressor gene, while subsequent chromosomal instability, characterized by mutations in KRAS and TP53 genes, as well as 18q loss of heterozygosity, drives the progression from normal epithelium to polyp formation and ultimately to cancer.[11–16] The primary role of telomeres is to safeguard the stability of chromosomes, whereby their shortening can directly contribute to chromosomal instability, potentially facilitating the development of CRC. Here, KRAS is linked to cancer.