The molecular biological pathogenesis of sporadic colorectal carcinoma, which includes most cases of colorectal cancer, involves activation of APC/β-catenin pathway, chromosomal instability of various oncogenes such as p53, DCC, and SMAD2/4, and microsatellite instability due to defective DNA mismatch repair gene and serrated pathways [2]. The gene discussed is DCC; the disease is colorectal cancer.