CSCs and EPCs exhibit high YAP and WNT signaling activity, driven by mutation of related genes, such as APC and KRAS, which has been identified to be critical for CRC tumorigenesis.[30, 50] CSCs may also develop through acquisition of stemness from differentiated cells by reprogramming during tumor progression.[51] CSCs have short telomeres but without further shortening, and this may be explained by their dormancy without cell proliferation, such that short telomeres do not undergo further shortening without telomerase. This evidence concerns the gene KRAS and colorectal carcinoma.