The reason for opting for KRAS over EpCAM was that (1) KRAS was closely related to CRC signaling pathways such as MAPK, PI3K, Wnt, and EGFR [103,104,105,106]; (2) almost half of the CRC patients were characterized by a mutation in the codons 12 and 13 in exon 2 of the KRAS gene [107,108]; and (3) those without the KRAS mutation tend to develop secondary KRAS mutations (~30%) during courses of targeted therapy [109,110]. This evidence concerns the gene EPCAM and colorectal carcinoma.